ENVIRONMENTAL RISK

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Adam Pawełczyk František Božek Marian Żuber

ENVIRONMENTAL RISK

CASE STUDIES

CZECH-POL TRADE Prague 2018

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Chris van KEER – University of Leuven, Belgium

Zoltan ZAVARGO – University of Novi Sad, Republic of Serbia

Cover design Piotr ŻUBER

All parts of this publication are protected by copyright law. It must not be used in any way without the consent of the Publisher. In particular, it must not be copied, translated, reproduced on microfilm or stored in or processed by electronic systems.

All violations will be prosecuted.

ISBN 978-80-907124-0-9

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List of Abbreviations

AD – Adults Exposure Duration

ADAF – Age Dependent Adjustment Factor ADD – Average Daily Dose

AT – Averaging Time

ATSDR – Agency for Toxic Substances and Disease Registry

BW – Body Weight

CALEPA – California Environmental Protection Agency CDI – Chronic Daily Intake

CERCLA – Congress Enacted the Comprehensive Environmental Response, Compensation, and Liability Act

COPs – Organochlorine Pesticides CPS – Carcinogenic Potency Strength CSF – Cancer Slope Factor

CSFo – Oral Cancer Slope Factor CSF_i – Inhalation Cancer Slope Factor EC – Exposure Concentration ED – Exposure Duration EF – Exposure Frequency ELCR – Excess Lifetime Cancer Risk

ET – Exposure Time

HEAST – Health Effects Assessment Summary Tables

HI – Hazard Index

HQ – Hazard Quotient

IARC – International Agency for Research on Cancer

IR – Intake Rate

IRIS – Integrated Risk Information System IUR – Inhalation Unit Risk

LADD – Lifetime Average Daily Dose

LOAEL – Lowest Observed Adverse Effect Level MCL – Maximum Contaminant Level

MF – Modifying Factor

MHC – Ministry of Health Care

MPC – Maximum Permissible Concentration MRE – Maximum Residential Exposures

NDEP – Nevada Division of Environmental Protection NOAEL – No Observed Adverse Effect Level

OEHHA – Office of Environmental Health Hazard Assessment

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PCBs – Polychlorinated Biphenyls PCM – Phase Contrast Microscopy PCOM – Phase-Contrast Optical Microscopy POPs – Persistent Organic Pollutants RAIS – Risk Assessment Information System RfC – Reference Concentration

RfD – Reference Dose

UF – Uncertainty Factor URF – Unit Risk Factor

US EPA – US Environmental Protection Agency WHO – World Health Organization

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1. Preface

Environmental risk is actual or potential hazard for living organisms and other elements of the environment that may exhibit adverse effects caused by effluents, emissions and waste materials, arising from human activities. Assessment of the health risk is a procedure within a scope of the environmental risk assessment. Estimation of the health risk comprises qualitative and quantitative evaluation of the human’s exposure to environmental contamination. On this basis probability of manifestation of adverse health effects in a population is determined. This work deals with the topics of assessment of risk for human health arising from environmental contamination.

Procedures of the environmental health risk assessment had been developed in the 1980s as a part of a Federal government effort to clean up land in the United States that was contaminated by hazardous waste and that was identified by the US Environmental Protection Agency (EPA). The program was created when Congress Enacted the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA).

Until that time the primary method of environmental hazard evaluation consisted in comparing the real contamination level with pollutants’ permissible concentrations in the air, water and soil. The highest permissible concentrations of the pollutants in the environment have been set out by the governments of particular countries in order to protect humans from possible exposition to harmful substances found in the air, water and soil.

Such an approach however, does not reflect the real health hazard level that the people are facing during their contact with the environment. In fact, the probability of health effects incidences caused by the pollutants depends not only on the arbitrarily adopted permissible concentrations but most of all on the exposure scenarios of the population considered. It is only the full analysis of actual health risk that shows real effects of the polluted environment on humans.

This book presents cases of the air, water and soil pollution with harmful substances, both toxic and mutagenic, and gives examples of hazard’s estimation as well as health risk assessment in different exposure scenarios. Residential and occupational scenarios are mostly taken into account. They include all elements of the procedure starting from hazard identification, followed by exposure assessment, determination of

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dose-response relation, risk characterization and ending with uncertainty analysis.

Also some recommendations in a concise manner are given aiming at hazard as well as health risk abatement.

The presented examples involve real, independent cases that were subjects to governmental grants and commercial projects. The cases aim to help the reader to understand more clearly different calculation methodologies and to carry out the risk assessment in different environments. The work focus are exclusively anthropogenic emissions released as a result of routine commercial businesses, municipal activities as well as technical disasters affecting human health and well-being. It should be stressed that there exist examples of the environmental pollution where, so far, no precise risk assessment is possible due to the lack of necessary data or reliable estimation procedures. Such a case could be contamination with petroleum products which usually constitute a mixture of hundreds chemical compounds of different chemical, physical and toxicological properties.

This book is intended as a selection of the representative cases describing risk estimation procedures, aimed at students, professionals and other users interested in disciplines ranging from environmental engineering and environmental chemistry to environmental safety and all areas of environmental science where human health and well-being are involved.

Adam Pawełczyk

This work was carried out at the Wrocław University of Science and Technology, Poland within the scientific funds allocated for statutory activities 0401/0200/17 by the Ministry of Science and Higher Education.

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2. Introduction to the risk assessment

2.1. Overview

The commonly accepted approach of environmental hazard assumes comparison of the real measured level of particular contaminants in the ambient environment with permissible pollution standards, set by the obligatory law regulations. In Poland the standards established by the Ministry of Environment control the pollution levels in the air, waters and soils (ME 2001). Additionally, for the purpose of the degraded grounds remediation, specific standards for soils and earth quality were laid down (ME 2002).

In the USA and some Western European countries environmental health risk assessment procedures have been implemented, enabling to determine probability of oc- currence of adverse health effects, resulting from the human’s exposure to the contaminated sites. This assessment constitutes a part of the risk management and is applied for establishing the strategy and actions aiming at the risk abatement (Wcislo 2003). The most applicable method of the risk reduction involves both the environment cleaning and harmful substances neutralization. Second possibility is elimination of exposure pathways. The third, most disputable way of the risk avoidance is limitation of the receptor’s access to the polluted area. It means that population from the polluted area has to be evacuated or the polluted area declared as a restricted access zone.

For the purpose of the health risk assessment related to polluted areas and for cleaning up projects a special federal government’s program has been declared in the USA named “Superfund”. The program needed a particular procedure of the health risk estimation which had not been developed at that time. The United States Envi- ronmental Protection Agency – US EPA started works on development of methodo- logical principles of the health risk assessment which could be an aid in taking any measures and actions addressed the contaminated sites problem. The methodology has been published in the Risk Assessment Guidance for Superfund (EPA 1989).

The methodology based on US EPA guidelines distinguishes the toxic and carcinogenic substances and recommends different approach in the risk assessment for

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both types of pollutants. Prior to the assessment procedure goal of the evaluation should be defined. The procedure results can be used for the selection of remedy actions, arbitration proceedings or it can be just a cognitive research. The methodology consists of the following main steps shown in Fig. 1: hazard identification, exposure assessment, dose–response assessment, risk characterization and uncertainty analysis.

Fig. 1. Sequence of the stages of the health risk assessment

The first step is a part of toxicity assessment characterizing the chemicals in respect of type and intensity of health effects resulted from the exposure to the chemicals. It enables to reduce number of chemicals to be considered in the risk assessment.

This step may include data collection and evaluation and comparison of site contamination with background and selects all data needed for use in the risk assessment.

Collection and evaluation of the data includes determination of humans’ contacts with the harmful chemicals, magnitude of exposures to the chemicals that are present in the environment and quantification of the exposure. The exposure exists only when three of the following elements exist at the same time: the exposure source, the exposure pathway and the receptor. This step usually takes into account current and future exposures considering different exposure pathways: inhalation (air), ingestion (water, meat, eggs, vegetables and dairy products) and dermal contact (contact with the soil, water,

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Introduction to the risk assessment 11

etc). As the receptor, an individual is meant. A necessary part of the exposure assessment is characteristics of the site and characteristics of the populations on the site.

Furthermore, quantification of exposure has to be conducted. The quantification includes calculation of chemicals’ intakes by the individual for each exposure pathway. The intakes are daily doses averaged over the lifetime or exposure duration, absorbed by a representative of certain population and are expressed in terms of the mass of substance in contact with the body per unit body weight per unit time (e.g. mg chemical substance per kg body weight per day – [mg/(kgday)]). Other approach consists in determination of chronic concentration instead of average doses absorbed. This refers mainly to inhalation exposure pathway. In this step an exposure scenario is very important as it determines the exposure time, contact frequency etc. Three basic scenarios are considered:

 resident’s scenario,

 incidental/recreational contact scenario,

 occupational scenario.

Next, physiological exposure factors such as age and gender should be considered depending on the type of population affected by the chemicals. These factors determine the body weight, contact frequency, the daily inhalation rate values, ingested water, food etc. For example standard procedures applied for the exposure calculations assume the body weight 78.1 kg for men, 65.4 kg for women and 16 kg for children of age between 1 and 6 years (EPA 2000). Also daily water intake and inhalation rates vary for different population groups.

The next step is determination quantitatively the relationship between the dose of the contaminant absorbed and the frequency of adverse health effects among the exposed population established. In the health risk assessment distinction between two types of hazardous chemicals is made – toxic (non-carcinogenic) and carcinogenic.

This step is followed by discussion of the level of calculated risk and hazards. The obtained figures are compared with commonly accepted risk levels. In the case of unaccepted hazards some solutions may be proposed in order to reduce risk.

The risk assessment procedure ends with uncertainty analysis that is a discussion of all possible inaccuracies and simplifying assumptions reflecting the calculated risk values and risk characterization. More detailed data are given in the chapters present- ing particular case studies.

2.2. Hazard identification

Hazard identification is a part of the whole procedure which is related to the identification if a substance present in the environment produces adverse health effects (e.g., cancer, allergy, birth defect) and whether the adverse health effects are likely to occur

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in humans. Type of the effects are recognized and their dependency on the level of absorbed doses. Findings of this stage are a determining factor in the taking of a deci- sion about further assessment steps.

2.3. Exposure assessment

Exposure assessment consists in determining doses of particular chemicals absorbed by the individuals over all pathways defined in the exposure scenarios. This step requires precise data on the contaminants concentration and population structure, especially when residents scenario is concerned. Calculations of the chemicals intake transported into the individual’s body by different exposure pathways can be conducted using equations recommended in the Risk Assessment Guidance for Superfund (EPA 1989). The universal formula for calculation of the intake of chemical can be expressed as:

I = C  CR  EFD/(BW  AT) (1)

where:

I – intake – amount of the chemical taken [mg(kg body weight)^-1d^–1], C – average concentration of the chemical over the exposure period, [mg/dm³

water], [mg/kg soil], [mg/m³ air], etc.,

CR – contact rate, amount of contaminated medium contacted per unit time, [mg soil/d], [m³ water /d], [m³ air/d], etc.,

EFD – exposure frequency and duration. It describes how often and how fre- quently exposure occurs [hours], [days], [years],

BW – average body weight [kg],

AT – averaging time, period over which exposure is averaged [d].

The exposure and risk assessment require establishing of exposure scenario models adjusted to the site and population characteristics. The scenarios enable to adapt formula (1) to the real cases of exposure, taking into consideration the following basic exposure pathways:

 ingestion of the water polluted with chemicals,

 inhalation of air containing toxic or carcinogenic substances,

 inhalation of air polluted with airborne dust originating from soil dusting,

 inhalation of air contaminated with volatile chemical substances released from the soil,

 consumption of vegetables and agricultural products grown on the polluted soil,

 consumption of meat and dairy products from animal breeding on the polluted area,

 incidental ingestion of the contaminated soil,

 dermal contact with the contaminated soil (EPA 1989).

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One should be aware that much more exposure scenarios are possible. They include a combination of the above pathways and number of other variants, resulting from the type of the receptor contact with the polluted medium. Thus, variety of specific formulas can be derived from the formula (1) enabling to calculate the chemicals intake for variety of pathways and exposure scenarios. Below some most used examples are given which may vary when real conditions are applied, depending on particular exposure scenario (EPA 1989).

Intake of chemicals by ingestion with drinking water

The amount of chemicals ingested with drinking water can be calculated from the formula:

I = Cw  IR  (EF  ED)/(BW  AT) (2) where:

Cw – average concentration of the chemical in water over the exposure period [mg/dm],

IR – ingestion rate – daily consumption of water [dm³/d], EF – exposure frequency [d/y],

ED – exposure duration [y], BW – average body weight [kg],

AT – averaging time, period over which exposure is averaged [d].

Intake of chemicals by inhalation with air

I = Ca  IR  ET  EF  ED/(BW  AT) (3) where:

Ca – average concentration of the chemical in air over the exposure period [mg/m³],

IR – inhalation rate [m³/h], ET – exposure time [h/d], the remaining symbols are the same.

Intake of chemicals by ingestion of contaminated fruits and vegetables

I = C_f  IR  FI  EF  ED/(BW  AT) (4) where:

Cf – average concentration of the chemical in food [mg/kg], IR – ingestion rate [kg/meal],

FI – fraction ingested from contaminated source – unitless, EF – exposure frequency [meals/y],

ED – exposure duration [y].

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Similar formula is applied for calculations of the chemicals intake by ingestion of contaminated meat, eggs and dairy products.

Intake of chemicals by accidental ingestion of contaminated soil

I = Cs  IR  CF  FI  EF  ED/(BW  AT) (5) where:

C_s – concentration of chemical in soil [mg/kg], IR – ingestion rate [mg soil/day],

CF – conversion factor [10^–6 kg/mg], EF – exposure frequency [d/y].

Absorbed dose of chemicals by dermal contact with the contaminated soil I = Cs  CF  SA  AF  ABS  EF  ED/BW  AT (6) where:

SA – skin surface area contacting with the soil [cm²/event], AF – soil to skin adherence factor [mg/cm²],

ABS – absorption factor – unitless, EF – exposure frequency [events/y].

The above examples illustrate some of cases from among numerous possibilities reflecting variety of exposure scenarios.

When calculating the intakes particular concern should be devoted to considerations of the exposure duration and averaging time. The standard exposure durations and averaging times are classified as chronic, subchronic and shorter-term exposures.

Applying the proper exposure and averaging time values has great weight for correct- ness of the whole risk assessment process. The averaging time which has to be chosen for exposure calculations depends on the type of pollutant – carcinogenic or non- carcinogenic – and on the type of toxic effect being assessed. Below the possible cases are given:

Toxic (non-carcinogenic) chemicals

In the case of non-carcinogenic substances the intakes are always determined by averaging them over the period of exposure, that is:

 developmental toxicants – when evaluation exposures to developmental toxicants is made, intakes are calculated by averaging over the exposure event, for instance over a day or a single exposure incident.

 acute toxic substances – for calculation of acute toxic substances intakes, the shortest exposure period that could produce an adverse effect is used for averaging. It is usually an exposure event or a day.

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 longer term exposure to non-carcinogenic toxicants (developmental and acute) – intakes are determined by averaging them over the period of exposure (i.e., subchronic or chronic daily intakes).

Generally the intake calculated in this way are called average daily dose (ADD).

Carcinogenic chemicals

For carcinogenic chemicals the intakes are calculated by proportional distribution of the total cumulative dose absorbed, over a lifetime. It is assumed for carcinogens that high doses of the chemicals absorbed by an individual over a short period of time is equivalent to corresponding low doses spread over a lifetime (EPA 1986b). It means that intakes are determined by averaging them over the lifetime, that is 70 years by convention (70 years  365 days/year = 25 550 days, actually). Such averaged intakes are called chronic daily intakes (CDI) or lifetime average daily doses (LADD).

2.4. Dose–response assessment

The dose–response assessment is a step in which toxicological and epidemiological knowledge is involved. In this step toxicity of the chemicals contaminating the environment is discussed and quantitatively relationship between the dose of the contaminant absorbed and the frequency of adverse health effects among the exposed population established. For the purpose of the dose–response assessment, toxicity data bases have been determined and published. The most useful are Integrated Risk In- formation Systems (IRIS), Risk Assessment Information System (RAIS), Agency for Toxic Substances and Disease Registry (ATSDR) and Health Effects Assessment Sum- mary Tables (HEAST). Use of these data bases substantially simplifies the assessment procedure. When no data are available, arduous, time consuming and very costly toxicological and epidemiological investigations are needed which in many cases makes the assessment impossible.

In the health risk assessment distinction between two types of hazardous chemicals is made – toxic (non-carcinogenic) and carcinogenic.

2.4.1. Toxic substances

Toxic substances are believed to comply with the threshold theory of toxicity while carcinogenic ones the linear theory. According to the threshold theory, a toxic chemical must be present in an organism at some threshold concentration, or a threshold dose must be absorbed before any adverse effects occur. It means that protective

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mechanisms are believed to exist in human organism that must be broken before the adverse effect appears. Below the threshold concentration or dose, no such adverse effects appear (Fig. 2).

Fig. 2. Threshold doses for toxic substances A, B and C

For evaluating the non-carcinogenic effects most often a “reference dose” (RfD) applies for exposure periods between 7 years (approximately 10 percent of a human lifetime) and a lifetime. RfD has been derived from the so called “no-observed- -adverse-effect-level” (NOAEL), that is from highest concentration (or dose) of a toxic substance, that produces no health effects yet. When the threshold concentration is exceeded the adverse effect start to manifest. Similarly the so called “lowest-observed- -adverse-effect-level” (LOAEL) is defined which is the lowest concentration (or dose) of a toxic substance that manifest health adverse effects.

The RfD incorporates “modifying factor” (MF) taking into account limited quality of data bases, extrapolation of doses from experimental models to real environmental conditions and uncertainty connected with transferring experimental data from animals to hu- mans. Additional “uncertainty factor” (UF) ranging from 0 to 10 is applied for purpose of safety margin (EPA 1989). It reflects additional uncertainties in health assessment procedure for non-carcinogenic substances. The RfD is calculated from:

RfD = NOAEL / (UF  MF). (7)

The unit for RfD is [mg/(kg d)].

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For such substances a non-probabilistic approach is used for evaluation of the potential health effects intensity. Instead, comparison of the absorbed dose by an individual over a specified time period, with the reference dose RfD derived for a similar exposure period is conducted. The calculated value is called a non-cancerous hazard quotient HQ which expresses how many times the exposure level (the dose taken) exceeds the RfD.

In other words HQ stands for the ratio of the exposure estimate to a concentration or dose, considered to represent a “safe” environmental concentration or dose RfD.

HQ = E/RfD (8)

where E – exposure level (intake).

The noncancer hazard quotient HQ assumes that there is a threshold level of expo- sure RfD below which adverse health effects will not develop. If the exposure E ex- ceeds this threshold (if E/RfD > 1), potential noncancer effects may occur. For consid- eration of the possibility of adverse noncarcinogenic health effects, three standard exposure durations are used:

– chronic (for humans they range in duration from 7 years to a lifetime), – subchronic (from 2 weeks to 7 years),

– shorter-term exposures (less than 2 weeks).

It should be stressed that for evaluation of short-term exposures and potential non- carcinogenic effects, subchronic or shorter-term, not chronic toxicity values RfD should be used.

In the case of exposure to several noncarcinogenic substances, the potential for the noncarcinogenic health effects is assessed in accordance with the principle of the cu- mulative effect of the chemicals on the body, by calculating a hazard index HI, being a sum of the hazard quotients determined for the individual substances:

HI = Σ HQi (9)

where: HQ_i – a hazard quotient for the i-th substance.

An HI exceeding 1 means that at a given exposure value harmful health effects may arise. Generally the following hazard level thresholds are specified in the literature (Brebbia 2010):

HQ  1 – acceptable HQ  (1; 4 – tolerable HQ  4 – unacceptable.

The same values are valid for Hazard index HI.

2.4.2. Carcinogens

Carcinogenic substances are believed to comply with linear theory (Fig. 3) that means that there are no threshold concentration levels safe for an individual. As

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opposed to toxic substances each dose of carcinogen, even lowest, may cause a cancer risk.

According to the classification developed by US EPA the following carcinogenic group have been established:

A – carcinogenic to humans: agents with adequate human data to demonstrate the causal association of the agent with human cancer (typically epidemiologic data).

B – probably carcinogenic to humans with two sub-groups:

B1 – agents with sufficient evidence from animal bioassay data, but either limited human evidence,

B2 – with little or no human data.

C – possibly carcinogenic to humans: agents with limited animal evidence and little or no human data.

D – not classifiable as to human carcinogenicity: agents without adequate data either to support or refute human carcinogenicity.

E – evidence of non-carcinogenicity for humans: agents that show no evidence for carcinogenicity in at least two adequate animal tests in different species or in both adequate epidemiologic and animal studies.

Fig. 3. Linear response to doses for carcinogenic substances X, Y and Z

Toxicity value for carcinogenic effects, or in other words a factor enabling to convert the absorbed dose of human carcinogen into cancer risk composes the so called

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“cancer slope factor” (CSF) or “carcinogenic potency strength” (CPS). The greater slope, the strongest carcinogenic effect may be expected. As shown in Fig. 2 the substance “A” has the greatest carcinogenic potency strength. Slope factors are calculated for carcinogens in classes A, B1, and B2 and are published in data bases of EPA. CFS is mostly expressed in [(mg/(kg d))^–1].

Toxicity values for carcinogenic effects can also be expressed in terms of risk per unit concentration of the chemical in the medium (air, water) being in contact with an individual. These risks per unit concentrations are called unit risks or unit risk factors (URF) and are calculated by dividing and multiplying the slope factor by standardized figures representing body weight and ingestion/inhalation rates. To get URF for ingestion of a substance with water, the oral cancer slope factor (CSFo) is divided by 70 kg (average adult body weight, as convention) and multiplied by 2 dm³/day (daily water consumption). Similarly, the URF for inhalation contact is obtained by dividing the inhalation cancer slope factor (CSF_i) by 70 kg and multiplied by 20 m³/day (daily air inhalation rate). Thus:

– water unit risk = risk per µg/dm³ = CSFo/70 (kg)2 [dm³/(day10^–3)], and – air unit risk = risk per µg/dm³ = CSF_i/70 (kg)20 [m³/(day10^–3)].

The multiplication factor 10^–3 is used to convert the units. CSF is expressed in [(mg/(kgday))^–1] while the unit risk is given in [µg/dm³] – for water unit risk, or in [µg/m³] – for air unit risk.

For cancer risks assessment, exclusively average lifetime exposure must be used.

On the other hand noncarcinogenic effects assessment is obligatory conducted using short-term exposures.

The following linear relation is used for the low-dose carcinogenic risk quantification (EPA 1999):

Risk = CSF  CDI (10)

where:

Risk – unitless cancer probability of developing cancer, CSF – slope factor, expressed in [(mg/(kgday))^–1].

CDI – chronic daily intake averaged over 70 years [mg/(kgday)] – ingested with drinking water, by inhalation with air, by ingestion of contaminated fruits and vegetables, by accidental ingestion of contaminated soil or by dermal contact with the contaminated soil, etc. CDI is also called the lifetime av- erage daily dose (LADD).

The linear equation (10) is valid only when low risk levels exist, that is below 0.01.

For higher exposure levels where higher risk is expected the following expression is valid:

Risk = 1 – e^{–(CDICSF)}. (11)

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Cancer risk for multiple substances can be calculated from the following equation:





 ^m

i

t Risk

Risk

1

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where:

Risk_t – the total cancer risk expressed as a unitless probability Riski – the risk estimate for the i-th substance.

The calculated risk represents the probability of cancer incidence above the natural level in the environment at particular site, caused by the contaminating chemical.

In the original guidelines developed by Superfund, a carcinogenic risk range of 110^–4 to 110^–7 modified to 110^–4 to 110^–6 was recommended as a target risk level.

Thus, the ambient chemical concentrations should be reduced to the levels providing at least the risk within the above mentioned limits (EPA 2015c; Kelly 1991).

The National Contingency Plan in the USA designated 10^–6 as a starting point for discussion of acceptable target risk at a site or as a “point of departure” (EPA 2015d).

This problem has generated a lot of debate in scientific papers and it still arouses con- troversies. Nevertheless, 10^–6 is now generally regarded by literature as acceptable and safe (Callahan 2004).

In general, the US EPA considers cancer risks that are below 1 chance in 1 000 000 (1 × 10^–6 or 1E–06) to be so small as to be negligible, and risks above 1E–04 to be suffi- ciently large that some sort of remediation is desirable. Excess cancer risks that range between 1E–06 and 1E–04 are generally considered to be acceptable.

2.5. Risk characterization

Risk characterization is an integral element of the risk assessment procedure for both ecological and health risks. The purpose of risk characterizations is to interpret the risk calculations and available data coming from observations and explain their meaning for the health of populations. Characterization is a kind of discussion and summarization of the whole assessment process which helps users understand findings of the risk estimation.

An important part of the risk characterization is comparison of the risk and hazard levels with generally accepted international acceptable target risks (Calla- han 2004, Brebbia 2010). The risk characterization is an essential component of the risk assessment process that supports judgment aiming at the risk abatement actions.

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2.6. Uncertainty analysis

The risk assessment procedure must absolutely end with uncertainty analysis that is a discussion of all possible inaccuracies and simplifying assumptions reflecting the calculated risk values and risk characterization. The uncertainties result from limita- tions of the toxicity information for many of the chemicals. The toxicity values are derived from experiments conducted with animals and extrapolated on human organisms. Consequently, there are varying degrees of uncertainty associated with the toxicity values calculated. The exposure parameters used in these risk calculations (hours/day, days/year) are based on some scenario assumptions which in many cases are not very accurate. Additionally it is not known whether concentrations of the harmful contaminants in the environment remain at a constant level over the whole lifetime of the individuals belonging to a given population. Usually the exposed human population is very diverse with respect of the gender, age, individual factors, and physiology. This reflects the daily inhalation, water and food ingestion which affects the contaminating chemical intake dose.

Also the sampling conditions are quite often not uniform in regard to the weather conditions at sampling sites. The concentrations may vary significantly depending on the weather parameters, and protective measures taken, which can lead to some uncertainty in the derived health risk values. Due to the simplifications and ambiguities the obtained results cannot be regarded as definite and absolute.

For reduction of the uncertainties computer-aided simulations have been implemented. They enable to carry out sensitivity analysis of the final results and to identify the crucial exposure pathways. Such extensive opportunities in evaluation of the uncertainty and variability associated with risk assessments for contaminated sites gives the Monte Carlo analysis (Hayse 2000). The probabilistic approach to the risk assessment with the use of Monte Carlo simulation involves the computational parameters in form of value distributions instead of point values. Thus, the Monte Carlo approach makes it possible to analyze the health risk in form of distribution curve providing the assessors with information about the relation risk level – population percentage concerned.

The following sections present case studies related to the real conditions and assessment procedures adapted and developed in frame of the authors’ research projects.

The above risk assessment procedures were applied with modifications and adjust- ments necessary to estimate and characterize the exposure and risk associated with environment contamination with organochlorine compounds, asbestos and nitrogen compounds. The contaminants origin represents all types of the pollution sources described in chapter 1, that is the running production (1-st type of source), stored waste materials and accumulated harmful products (2-nd type of source) and emission as a consequence of accidents (3-rd type of source).

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A few words should be devoted to the cases related to the environment pollution with complex mixtures, petroleum products, for instance. So far, there was no precise risk quantification method developed for such systems. This is due to lack of adequate knowledge about the movement of petroleum components in soil and shortage of data about the toxicity of the components. The available analytical methodology does not provide adequate information necessary to evaluate the health risks posed to humans by the mixtures of complex nature (Grabas et al. 2015; Heath et al. 1993; Pawełczyk et al. 2017a; Todd et al. 1999).

Thus, health risk assessment in those cases is rather impossible. Some approaches consist in defining reference compounds of relatively well characterized toxicity for a range of compounds. For example, for unsaturated compounds, one reference RfD was identified for all compounds C9 through C32. For this group of hydrocarbons pyrene was accepted as reference compound with RfD 0.03 mg/kg/day (Hutcheson et al. 1996).

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3. Cases overview

Case studies presented in this book cover different instances of the environment polluted with harmful substances that found their way to air, waters and soils on mili- tary and civilian areas. A brief profiles of particular cases are presented hereafter.

As mentioned in the preface, exclusively man-made emissions that happened as a consequence of routine commercial businesses, municipal activities as well as technical disasters affecting human health and well-being have been considered (Yung-Tse Hung et al. 2012; Maciejewski and Żuber 2006).

Occupational risk posed by soil contaminants. The case study concerns estimation of the health risk in the occupational scenario on a delimitated property intended for railway carriage service station. The estimation comprises assessment of ground contamination data, toxicological assessment of the identified anthropogenic pollutants, identification of the environmental hazard, exposure assessment in the occupational scenario, estimation of dose-response relation, risk characterization and uncertainty analysis.

The assessment comprises qualitative and quantitative determination of the humans exposure to environmental contamination. On this basis probability of manifestation of adverse health effects in a population is determined.

In the procedure of occupational health risk assessment an exposure to upper layer of the polluted soil was taken into account. Inhalation route of exposure was not considered because there were no circumstances for the presence of harmful anthropogenic substances in the air in significant concentrations. Ground waters had not been taken into consideration, as well, for in the assumed scenarios no contact of the station staff occurs with this exposure source.

Chromium in the environment. In this case study the results of water, soil and air analyses sampled in the vicinity of a former ferrochromium metallurgical plant. In the past, the area was used for the disposal of waste materials containing smelter slag, dust and other waste products from the manufacture of ferrochromium alloys for the army.

In nineties, the production was abandoned and a project aimed at the liquidation of the dump had been initiated. The project concentrated on the recovery of chromium re- mains and the utilization of the leftover material as a road construction aggregate.

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Based on the analyses of ground water, soil and air, a health risk caused by environmental pollution with chromium, especially with Cr(VI), was determined for residential and occupational scenarios. It was found that the level of chromium emissions to the environment constitutes a potential danger of toxic and carcinogenic cases in humans exposed to the emission in the affected area. An increased level in the hazard quotient has been observed in the case of occupational activities. As far as the mutagenic effects are concerned, the occupational inhalation exposure was found to be very high, which may raise extreme concern about carcinogenic risk.

Surface waters contaminated with nitrogen compounds. Results of analyses of water in the river Mała Panew in South West Poland have been reported. The river flows through a rural area with some chemical industry developed. Aim of the work was to investigate the pollutants level in the river, compare the obtained results with obligatory drinking water standards and determine possible health effects when using the river as a source for drinking water production. Attention was put to nitrogen compounds as nitrate(V) ions (NO³⁻) and nitrite(III) ions (NO²⁻), mostly of anthropogenic origin were detected in the monitored water. The average concentrations of the NO^3– and NO^2– were 3.54 mg/dm³ and 0.286 mg/dm³, respectively. The chances for non-carcinogenic effects, namely methemoglobinemia, resulting from possible exposure to the examined chemicals were determined based on the analytical and toxicological data. Since infants are the subpopulation most susceptible to nitrate induced methemoglobinemia, the assessment was limited to children aged 0–3 years. The de- termined values expressed by hazard quotient (HQ) and hazard index (HI) indicate that the water pollutants and their concentrations do not exceed unity, however in the case of infants, the other nitrate sources should be controlled.

Polychlorinated biphenyls in drinking water. This case study refers to water in- takes providing one of the districts located near the city of Wrocław with drinking water. Surprisingly high concentrations of polychlorinated biphenyls (PCBs) and or- ganochlorine pesticides (COPs), classified as persistent organic pollutants (POPs), were detected in the monitored sites. Based on the analytical and toxicological data, the individual health risks in respect to carcinogenic effects (excess cancer risk over a lifetime) in humans were assessed, resulting from direct ingestion of community water. Non-carcinogenic effects resulting from exposure to the examined POPs were determined, as well. The conservative approach to risk assessment, taking into account a safety margin for data incompleteness, was adopted. The carcinogenic risk was found to slightly exceed the unconditionally acceptable risk of 10–6 in the case of polychlorinated biphenyls and hexachlorocyclohexane (HCH), for all the inhabitant populations. The determined values of non-carcinogenic effects expressed by hazard quotient (HQ) and hazard index (HI) indicate that the water pollutants and their con- centrations do not cause an increase in non-carcinogenic incidences in the inhabitants using the monitored water sources.

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Cases overview 25

Asbestos in the air. This case study refers to an assessment of human health risk associated with the air pollution with asbestos respirable fibers in towns of the south- west Poland. The aim of the work was to determine if any prevention measures would be necessary to reduce the exposure of populations to the air pollutant. The risk assessment was carried out based on the air analyses and latest asbestos toxicity data published by the Environmental Protection Agency (US EPA), USA and Office of Environmental Health Hazard Assessment (OEHHA). It was found that in some sites the concentration of the asbestos fibers exceeded the acceptable levels, however it does not result in worrying health risk increase, even when the resident exposure scenario is taken into consideration. The highest asbestos fibers’ concentration was found in the air in the town centers during rush hours. In three spots however, the calculated maximum health risk exceeded 1E–04 which is generally considered high according to US EPA standards.

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4. Analytical methods

Chromium in the soil

The Polish Standard (PS, 1984) was adapted for sampling using a Quick Take 30 aspirator with an electronic flow control adjustment at the flow rate of 16.0 L/min and with 180 minutes sampling time applied. The air stream was filtered on Sartorius cellulose nitrate membrane filters with 25 mm diameter and 0.4 µm pores. After sampling, the filters were protected in plastic boxes and delivered to the laboratory.

Analyses of chromium in the samples were carried out by the ICP method using an ICP-MS spectrometer Elan 9000 Perkin Elmer. For mineralization of the samples, pressure decomposition in nitric acid and hydrogen peroxide was applied by the use of a microwave mineralizer Anton-Paar PE Multiwave 3000.

For the analysis of hexavalent chromium, a procedure described in Ashley et al.

(2003) was applied. Ion chromatography was used to separate Cr(VI). The equipment consisted of an HPLC PE series 200 with UV-Vis 785A and FD200, IC Dionex DX-120.

The mobile phase flow rate was 1.0 cm³/min, a post-column reagent flow rate was 0.7 cm³/min, and a post-column tube length was 2.2 m. The extraction was made with a 2% NaOH and a 3% Na₂CO₃solution in deionized water. The mobile phase was 250 mM (NH₄)2SO4 and 100 mM NH4OH.

The detection limit of chromium(VI) in the case of air samples was 0.004 μg per sample. For the ground water, it was about 1 μg/L, and for soil, it was about 5 μg/kg.

Polychlorinated biphenyls in water

The adapted analytical procedures according to the Polish Standards (PS 2002) were applied for determination of the examined pollutants in water. After a standard solution was added, double extraction with n-hexane was performed. Each sample was purified by adding sulfuric acid, shaking and separating the layers. The extract was dried by filtering it through a layer of sodium sulfate into a round-bottom flask, and concentrated (Pawełczyk et al. 2008).

Then a potassium hydroxide solution was added, the sample was heated and ethyl alcohol was introduced. After re-shaking the n-hexane layer was separated. The extracted and purified samples were analyzed using an M504 gas chromatograph

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equipped with an HP5 capillary column and an ECD electron capture selective to- wards organochlorine compounds. To heighten the detectability range sensibility of the apparatus was adjusted. The chromatograph’s operating parameters are shown in Table 1.

Table 1. Parameters of chromatographic apparatus

Parameter Value/type

column length 60 m

column temperature:

 initial

 temperature rise

 final

160 °C 5 °C/min

325 °C

initial isotherm 1 min

final isotherm 15 min

carrier gas nitrogen

doping gas nitrogen

Hydrocarbons in water and soil

Benzene, toluene, ethylbenzene and xylene (BTEX) were determined using a head- space gas chromatographic method. 0.5 dm³ of the water sample was extracted with 1 cm³ of n-pentane in a micro extraction flask according to the Polish Standard PN-85/C 04577. Simultaneously the sample was treated with ultra sounds for 10 min.

After separation the layers obtained were analyzed chromatographically.

The GC analyses of the extracts were carried out according to the Polish Standard PN-89/ C-04577 using gas chromatograph N-504 equipped with NUCOL capillary column, 30 m, 0.25 μm at 60 C. Isotherm was 8 min, temperature increment ranged between 5 C/min to 220 C, detector FID. The chromatograph was coupled with computer registration and data processing system KSPD Metroster. In the case of doubtful results and very small amounts of analytes the analyzes were performer using HPLC method. A column 4 mm was applied and phase C18 of Knauer company in isocratic conditions using eluent composed of 20% water and 80% methanol, detector UV, 254 nm, flow rate 1 cm³.

Nitrogen in water

After taking the samples they were put into the glass bottles and fixed by acidi- fying with HCl to pH 1–2 and cooled down to temperature about 5 °C. The samples were then delivered to the laboratory. Analyses of nitrate nitrogen were carried out using the colorimetric method while the nitrite nitrogen was determined by the molecular absorption spectroscopy according to (PSa) and (PSb), respectively.

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Analytical methods 29

Airborne asbestos

The air samples were collected according to adapted Polish Standard (PS 1984) and (Božek et al. 2016) using Quick Take 30 aspirator with an electronic flow control adjustment at the flow rate of 16.0 dm³/min and with 110 minutes sampling time applied.

The air stream was filtered on Sartorius cellulose nitrate membrane filters type 113, with 25 mm diameter and 0.8 µm pores. After sampling the filters were protected in boxes and delivered to the laboratory.

Prior to the microscopic examinations the filters were treated with diethyl oxalate/dimethyl phthalate balsam in order to make them transparent. The fibrous pollutants were identified and counted using the phase-contrast optical microscopy PCOM, according to (PS 1988). The fiber counts from the measurements composed a basis for further health risk assessment.

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5. Occupational risk

posed by soil contaminants

5.1. Background

The case concerns estimation of the health risk in the occupational scenario on a delimitated property used by engineers and other skilled workers employed as railway carriage servicemen. The estimation comprises the following elements:

 assessment of ground contamination data,

 toxicological assessment of the identified anthropogenic pollutants,

 identification of the environmental hazard,

 exposure assessment in the occupational scenario,

 estimation of dose–response relation,

 risk characterization,

 uncertainty analysis.

Assessment of the health risk is a procedure within a scope of the environmental risk assessment. Estimation of the health risk comprises qualitative and quantitative assessment of the humans exposure to environmental contamination.

On this basis probability of manifestation of adverse health effects in a population is determined.

In the procedure of occupational health risk assessment an exposure to upper layer of the polluted soil was taken into account. Inhalation route of exposure was not considered because there were no circumstances for the presence of harmful anthropogenic substances in the air in significant concentrations. Ground waters had not been taken into consideration, as well, for in the assumed scenarios no contact of the station staff occurs with this exposure source.

The scope of the evaluation reflects the premises characteristics, use regime, type of contamination and quality of analytical data. Risk assessment has been carried out based on the US Environmental Protection Agency (US EPA) published in the docu- ment Risk Assessment Guidance for Superfund. The latest toxicological data and procedures of risk assessment have been applied, as well. The applied methodology of the

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environmental risk estimation on the contaminated area is based on guidelines published in the frame of American governmental project “Superfund” (EPA 1980).

Guidelines developed by Agency for Toxic Substances and Disease Registry were taken into account, as well (ATSDR 2005).

In the considerations related to the exposure, legislation in force in Poland was taken into account which relates to soils, ground waters and all kind of the environmental pollution (ME 2002, ME 2008).

5.2. The site characterization

The considered facility is a delimitated property which is a part of a bigger com- plete service infrastructure. It has a shape of slightly bent Wedge about 650 meters long and 80 m wide (at its widest points). It is fitted with infrastructure intended for railway carriage service. Figure 4 presents aerial view of the station with the indicated ground and water sampling spots. In total 8 soil sampling points and 4 water sampling points were installed. There are railway tracks, service hall, communication tracks and other devices in the area.

Fig. 4. Aerial view of the facility with the indicated ground and water sampling spots

Access to the area was provided for the regular staff and subcontractors. Profes- sional activities connected with the rolling stock service and particularly with inspec-

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Occupational risk posed by soil contaminants 33

tion of the train chassis are carried out irregularly, in periods determined by railway accessibility. Exposure of the staff to the contaminants present in this area is a consequence of a contact with the soil.

The geomorphology of the soils is unknown. Thus, it was not possible to determine hazards posed by the contaminants migration from the Surface of the considered area to water bearing levels. The detected pollutants are of anthropogenic origin.

5.3. Starting data

In the assessment procedure the pollutants have been taken into account which most probably are present in the soil. They were identified based on the history and features of the area which in the past was and still is used by entities related to rail- ways. The following contaminants have been detected in the soil: arsenic, barium, cadmium, cobalt, chromium, copper, molybdenum, nickel, lead, tin, zinc, mercury, gasolines (hydrocarbons C6–C12), mineral oil, (hydrocarbons C12–C35), benzene, ethylbenzene, toluene, styrene, m-, p-, o-xylene, naphthalene, phenanthrene, anthracene, fluoranthene, chrysene, benzo(a)anthracene, benzo(a)pyrene, benzo(a)fluoranthene, benzo(g,h,i)perylene.

Table 2 presents analyses of the soil samples collected from 8 sites from different depths in the range between 0.0–0.3 m do 3.1–3.6 m.

Analyses of phenols showed minimum concentrations of monochlorophenol, di- chlorophenols, trichlorophenols, tetrachlorophenols and pentachlorophenols in the soil. None of the concentrations exceeds 0,1 mg/kg.

It should be noted that in the environment al analytics differentiation among chemical forms of the same element is often neglected. From the point of view of the environmental health risk assessment such proceedings are a drawback which makes it impossible to estimate health risk precisely. In the case of chromium, for instance, absence of speciation analysis distinguishing Cr(0), Cr(II) and Cr(VI) should be quali- fied as a serious mistake. This is due to drastic differences in toxicity of these three chromium forms. In such a case a conservative approach to risk assessment should be applied which legitimates use of Cr(VI) toxic values, that is the most harmful chemical form of this element.

Due to the lack of the speciation analysis of the metal forms in the environment the conservative approach was applied in this work. As a result certain overesti- mation of the calculated risk may be expected. Until the risk values are acceptable no repeated calculations and iteration are necessary to approach more real values of the risk.

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Table 2. Analyses of the soil with respect of metals and hydrocarbons concentration (gasolines, mineral oils, BTEX, PAH) (PIG 2016)

Sample No. 01 02 03 04 05 06 07 08

Dry mass 91.9 97 91.1 95.8 91.2 94.4 89.9 92.2

Metals

Arsenic (As) 2.62 <2 2.59 2.25 2.33 <2 2.76 <2

Barium (Ba) 53.4 <20 44.5 <20 40.2 <20 40.6 <20

Cadmium (Cd) <0.25 <0.25 0.333 <0.25 <0.25 <0.25 <0.25 <0.25

Cobalt (Co) 2.72 <2 <2 <2 2.1 <2 <2 <2

Chromium (Cr) 9 <5 7.87 <5 7.06 <5 6.52 <5

Copper (Cu) 19.6 <2 11.1 2.57 16.3 <2 7.81 <2

Molybdenum (Mo) <1 <1 <1 <1 <1 <1 <1 <1

Nickel (Ni) 6.02 1.1 3.92 1.48 3.81 <1 2.77 1.18

Lead (Pb) 21.6 <2 23.3 4.18 18.4 2.74 17.7 2.08

Tin (Sn) 5.79 <1 <1 <1 1.38 <1 <1 <1

Zinc (Zn) 85 <10 81.1 <10 52.2 <10 43.9 <10

Mercury (Hg) 0.0334 <0.0050 0.0583 0.0151 0.0404 0.0089 0.0361 0.0195 Aggregated parameters

Gasolines, total

(hydrocarb. C6–C12) <0.8 <0.8 <0.8 <0.8 <0.8 <0.8 <0.8 <0.8 Mineral oil

(hydrocarb. C12–C35) 15 <6 10 <6 12 <6 <6 <6

Volatile aromatic hydrocarbons (BTEX)

Benzene <0.01 <0.01 <0.01 <0.01

Ethylbenzene <0.01 <0.01 <0.01 <0.01

Toluene <0.01 <0.01 <0.01 <0.01

Styrene <0.01 <0.01 <0.01 <0.01

m-, p-, o-xylene <0.03 <0.03 <0.03 <0.03

BTEX, total <0.07 <0.07 <0.07 <0.07

Polyaromatic hydrocarbons (PAH)

Naphthalene 0.007 <0.005 <0.005 <0.005 0.006 <0.005 0.01 <0.005 Fenantrene 0.063 <0.005 0.032 0.014 0.059 <0.005 0.022 <0.005 Anthracene 0.026 <0.005 0.015 0.007 0.023 <0.005 0.012 <0.005

Fluoranthene 0.181 0.007 0.1 0.032 0.17 0.01 0.064 <0.005

Chrysene 0.108 <0.005 0.069 0.018 0.104 0.006 0.055 <0.005

Benzo(a)anthracene 0.092 <0.005 0.057 0.015 0.087 <0.005 0.038 <0.005 Benzo(a)pyrene 0.122 <0.005 0.07 0.019 0.109 0.006 0.051 <0.005 Benzo(a)fluoranthene 0.03 <0.005 0.017 <0.005 0.027 <0.005 0.011 <0.005 Benzo(g,h,i)perylene 0.1 <0.005 0.055 0.015 0.086 <0.005 0.037 <0.005 9 PAH, total 0.729 <0.045 0.415 0.12 0.671 <0.045 0.3 <0.045

ENVIRONMENTAL RISK

Adam Pawełczyk František Božek Marian Żuber