Dose-Response and Risk Assessment of Airborne Hexavalent Chromium and Lung Cancer Mortality

This study evaluates the dose-response relationship for inhalation exposure to hexavalent chromium [Cr(VI)] and lung cancer mortality for workers of a chromate production facility, and provides estimates of the carcinogenic potency. The data were analyzed using relative risk and additive risk dose-response models implemented with both Poisson and Cox regression. Potential confounding by birth cohort and smoking prevalence were also assessed. Lifetime cumulative exposure and highest monthly exposure were the dose metrics evaluated. The estimated lifetime additional risk of lung cancer mortality associated with 45 years of occupational exposure to 1 microg/m3 Cr(VI) (occupational exposure unit risk) was 0.00205 (90%CI: 0.00134, 0.00291) for the relative risk model and 0.00216 (90%CI: 0.00143, 0.00302) for the additive risk model assuming a linear dose response for cumulative exposure with a five-year lag. Extrapolating these findings to a continuous (e.g., environmental) exposure scenario yielded an environmental unit risk of 0.00978 (90%CI: 0.00640, 0.0138) for the relative risk model [e.g., a cancer slope factor of 34 (mg/kg-day)-1] and 0.0125 (90%CI: 0.00833, 0.0175) for the additive risk model. The relative risk model is preferred because it is more consistent with the expected trend for lung cancer risk with age. Based on statistical tests for exposure-related trend, there was no statistically significant increased lung cancer risk below lifetime cumulative occupational exposures of 1.0 mg-yr/m3, and no excess risk for workers whose highest average monthly exposure did not exceed the current Permissible Exposure Limit (52 microg/m3). It is acknowledged that this study had limited power to detect increases at these low exposure levels. These cancer potency estimates are comparable to those developed by U.S. regulatory agencies and should be useful for assessing the potential cancer hazard associated with inhaled Cr(VI).     

Microenvironmental Analysis of Residential Exposure to Chromium-Laden Wastes in and Around New Jersey Homes

The purpose of this study was to identify the significant microenvironments that can lead to chromium exposure in Hudson County, New Jersey residential settings near or on soil contaminated with chromium waste. Measurements were made in indoor air, outdoor air, and house dust. Surface dust was found to be the best index of potential Cr exposure. The values of Cr in Hudson County household dust ranged from 3.25-320 ng/cm2 in wipe samples and 1.0-12 ng/cm2 in vacuum samples. Elevated Cr in household dust was found to be related to residential locations near large chromium waste sites, household cleaning habits, and house renovation activities. Outdoor Cr air levels were similar to those obtained in other urban areas at these seasons of the year, approximately 5-7 ng/m3. Comparisons with measurements of the Cr levels in urine found that the elevated Cr in dust was associated with elevated excretion of Cr. Site-specific Cr differences in household dust suggest different sources and routes of exposure. Within the total group of homes in the present study, Cr in household dust was the major influence on household exposure.     

Cancer Risk Estimation for Mixtures of Coal Tars

Two-year chronic bioassays were conducted by using B6C3F1 female mice fed several concentrations of two different mixtures of coal tars from manufactured gas waste sites or benzo(a)pyrene (BaP). The purpose of the study was to obtain estimates of cancer potency of coal tar mixtures, by using conventional regulatory methods, for use in manufactured gas waste site remediation. A secondary purpose was to investigate the validity of using the concentration of a single potent carcinogen, in this case benzo(a)pyrene, to estimate the relative risk for a coal tar mixture. The study has shown that BaP dominates the cancer risk when its concentration is greater than 6,300 ppm in the coal tar mixture. In this case the most sensitive tissue site is the forestomach. Using low-dose linear extrapolation, the lifetime cancer risk for humans is estimated to be: Risk < 1.03 × 10⁻⁴ (ppm coal tar in total diet) + 240 × 10⁻⁴ (ppm BaP in total diet), based on forestomach tumors. If the BaP concentration in the coal tar mixture is less than 6,300 ppm, the more likely case, then lung tumors provide the largest estimated upper limit of risk, Risk < 2.55 × 10⁻⁴ (ppm coal tar in total diet), with no contribution of BaP to lung tumors. The upper limit of the cancer potency (slope factor) for lifetime oral exposure to benzo(a)pyrene is 1.2 × 10⁻³ per μg per kg body weight per day from this Good Laboratory Practice (GLP) study compared with the current value of 7.3 × 10⁻³ per μg per kg body weight per day listed in the U.S. EPA Integrated Risk Information System.     

A Monte Carlo Risk Assessment Model for Acrylamide Formation in French Fries

The objective of this study is to estimate the likely human exposure to the group 2a carcinogen, acrylamide, from French fries by Irish consumers by developing a quantitative risk assessment model using Monte Carlo simulation techniques. Various stages in the French-fry-making process were modeled from initial potato harvest, storage, and processing procedures. The model was developed in Microsoft Excel with the @Risk add-on package. The model was run for 10,000 iterations using Latin hypercube sampling. The simulated mean acrylamide level in French fries was calculated to be 317 μg/kg. It was found that females are exposed to smaller levels of acrylamide than males (mean exposure of 0.20 μg/kg bw/day and 0.27 μg/kg bw/day, respectively). Although the carcinogenic potency of acrylamide is not well known, the simulated probability of exceeding the average chronic human dietary intake of 1 μg/kg bw/day (as suggested by WHO) was 0.054 and 0.029 for males and females, respectively. A sensitivity analysis highlighted the importance of the selection of appropriate cultivars with known low reducing sugar levels for French fry production. Strict control of cooking conditions (correlation coefficient of 0.42 and 0.35 for frying time and temperature, respectively) and blanching procedures (correlation coefficient −0.25) were also found to be important in ensuring minimal acrylamide formation.     

An Exposure Assessment of Methyl Mercury via Fish Consumption for the Japanese Population

The objective of this article was to propose an exposure assessment model to describe the relationship between fish consumption and body methyl mercury (MeHg) levels in the Japanese population. Individual MeHg intake was estimated by the summation of species-specific fish consumption multiplied by species-specific fish MeHg levels. The distribution of fish consumed by individuals and the MeHg level in each fish species were assigned based on published data from Japanese government institutions. The probability of MeHg intake for a population was accomplished through a Monte Carlo simulation by the random sampling of fish consumption and species-specific MeHg levels. Internal body MeHg levels in blood and hair were estimated using a one-compartment model. Overall, the mean value of MeHg intake for the Japanese population was estimated to be 6.76 μg/day or 0.14 μg/kg body weight per day (bw/day), while the mean value for the hair mercury level was 2.02 μg/g. Compared with the survey data that tabulated hair mercury levels in a cross-section of the Japanese population, the simulation results matched the hair mercury survey data very well for women, but somewhat underestimated for men and all of the population. This exposure assessment model is a useful attempt at further risk assessment with respect to a risk-benefit analysis.     

Re-evaluation of the Reference Dose for Methylmercury and Assessment of Current Exposure Levels

Methylmercury (Me-Hg) is widely distributed through freshwater and saltwater food chains and human consumption of fish and shellfish has lead to widespread exposure. Both the U.S. EPA Reference Dose (0.3 μg/kg/day) and the FAO/WHO Permissible Tolerable Weekly Intake (3.3 μg/kg/week) are currently based on the prevention of paraesthesia in adult and older children. However, Me-Hg exposure in utero is known to result in a range of developmental neurologic effects including clinical CNS symptoms and delayed onset of walking. Based on a critical review of developmental toxicity data from human and animal studies, it is concluded that current guidelines for the prevention of paraesthesia are not adequate to address developmental effects. A dose of 0.07 μ/kg/day is suggested as the best estimate of a potential reference dose for developmental effects. Data on nationwide fish consumption rates and Me-Hg levels in fish/seafood weighted by proportion of the catch intended for human consumption are analyzed in a Monte Carlo simulation to derive a probability distribution of background Me-Hg exposure. While various uncertainties in the toxicologic and exposure data limit the precision with which health risk can be estimated, this analysis suggests that at current levels of Me-Hg exposure, a significant fraction of women of childbearing age have exposures above this suggested reference dose.     

Using Probabilistic Modeling to Evaluate Human Exposure to Organotin in Drinking Water Transported by Polyvinyl Chloride Pipe

The leaching of organotin (OT) heat stabilizers from polyvinyl chloride (PVC) pipes used in residential drinking water systems may affect the quality of drinking water. These OTs, principally mono- and di-substituted species of butyltins and methyltins, are a potential health concern because they belong to a broad class of compounds that may be immune, nervous, and reproductive system toxicants. In this article, we develop probability distributions of U.S. population exposures to mixtures of OTs encountered in drinking water transported by PVC pipes. We employed a family of mathematical models to estimate OT leaching rates from PVC pipe as a function of both surface area and time. We then integrated the distribution of estimated leaching rates into an exposure model that estimated the probability distribution of OT concentrations in tap waters and the resulting potential human OT exposures via tap water consumption. Our study results suggest that human OT exposures through tap water consumption are likely to be considerably lower than the World Health Organization (WHO) "safe" long-term concentration in drinking water (150 μg/L) for dibutyltin (DBT)—the most toxic of the OT considered in this article. The 90th percentile average daily dose (ADD) estimate of 0.034 ± 2.92 × 10⁻⁴μg/kg day is approximately 120 times lower than the WHO-based ADD for DBT (4.2 μg/kg day).     

Equation reliability of soil ingestion estimates in mass-balance soil ingestion studies

Exposure to chemicals from ingestion of contaminated soil may be an important pathway with potential health consequences for children. A key parameter used in assessing this exposure is the quantity of soil ingested, with estimates based on four short longitudinal mass-balance soil ingestion studies among children. The estimates use trace elements in the soil with low bioavailability that are minimally present in food. Soil ingestion corresponds to the excess trace element amounts excreted, after subtracting trace element amounts ingested from food and medications, expressed as an equivalent quantity of soil. The short duration of mass-balance studies, different concentrations of trace elements in food and soil, and potential for trace elements to be ingested from other nonsoil, nonfood sources contribute to variability and bias in the estimates. We develop a stochastic model for a soil ingestion estimator based on a trace element that accounts for critical features of the mass-balance equation. Using results from four mass-balance soil ingestion studies, we estimate the accuracy of soil ingestion estimators for different trace elements, and identify subjects where the difference between Al and Si estimates is larger (>3 RMSE) than expected. Such large differences occur in fewer than 12% of subjects in each of the four studies. We recommend the use of such criteria to flag and exclude subjects from soil ingestion analyses.     

Daily Soil Ingestion Estimates for Children at a Superfund Site

Ingestion of contaminated soil by children may result in significant exposure to toxic substances at contaminated sites. Estimates of such exposure are based on extrapolation of short-term-exposure estimates to longer time periods. This article provides daily estimates of soil ingestion on 64 children between the ages of 1 and 4 residing at a Superfund site; these values are employed to estimate the distribution of 7-day average soil ingestion exposures (mean, 31 mg/day; median, 17 mg/day) at a contaminated site over different time periods. Best linear unbiased predictors of the 95th-percentile of soil ingestion over 7 days, 30 days, 90 days, and 365 days are 133 mg/day, 112 mg/day, 108 mg/day and 106 mg/day, respectively. Variance components estimates (excluding titanium and outliers, based on Tukey's far-out criteria) are given for soil ingestion between subjects (59 mg/day)2, between days on a subject (95 mg/day)2, and for uncertainty on a subject-day (132 mg/day)2. These results expand knowledge of potential exposure to contaminants among young children from soil ingestion at contaminated sites. They also provide basic distributions that serve as a starting point for use in Monte Carlo risk assessments.     

Evaluating the Risk of Liver Cancer in Humans Exposed to Trichloroethylene Using Physiological Models

Trichloroethylene (TCE) is a widespread environmental pollutant. TCE is classified as a rodent carcinogen by the U.S. Environmental Protection Agency (EPA). Using the rodent cancer bioassay findings and estimates of metabolized dose, the EPA has estimated lifetime exposure cancer risks for humans that ingest TCE in drinking water or inhale TCE. In this study, a physiologically based pharmacokinetic (PB-PK) model for mice was used to simulate selected gavage and inhalation bioassays with TCE. Plausible dose-metrics thought to be linked with the mechanism of action for TCE carcinogenesis were selected. These dose-metrics, adjusted to reflect an average amount per day for a lifetime, were metabolism of TCE (AMET, mg/kg/day) and systemic concentration of TCA (AUCTCA, mg/L/day). These dose-metrics were then used in a linearized multistage model to estimate AMET and AUCTCA values that correspond to liver cancer risks of 1 in 1 million in mice. A human PB-PK model for TCE was then used to predict TCE concentrations in drinking water and air that would provide AMET and AUCTCA values equal to the predicted mice AMET and AUCTCA values that correspond to liver cancer risks of 1 in 1 million. For the dose-metrics, AMET and AUCTCA, the TCE concentrations in air were 10.0 and 0.1 ppb TCE (continuous exposure), respectively, and in water, 7 and 4 μg TCE/L, respectively.     

Physiological Daily Inhalation Rates for Health Risk Assessment in Overweight/Obese Children,Adults, and Elderly

Physiological daily inhalation rates reported in our previous study for normal‐weight subjects 2.6–96 years old were compared to inhalation data determined in free‐living overweight/obese individuals (n = 661) aged 5–96 years. Inhalation rates were also calculated in normal‐weight (n = 408), overweight (n = 225), and obese classes 1, 2, and 3 adults (n = 134) aged 20–96 years. These inhalation values were based on published indirect calorimetry measurements (n = 1,069) and disappearance rates of oral doses of water isotopes (i.e., ²H₂O and H₂¹⁸O) monitored by gas isotope ratio mass spectrometry usually in urine samples for an aggregate period of over 16,000 days. Ventilatory equivalents for overweight/obese subjects at rest and during their aggregate daytime activities (28.99 ± 6.03 L to 34.82 ± 8.22 L of air inhaled/L of oxygen consumed; mean ±  SD) were determined and used for calculations of inhalation rates. The interindividual variability factor calculated as the ratio of the highest 99th percentile to the lowest 1st percentile of daily inhalation rates is higher for absolute data expressed in m³/day (26.7) compared to those of data in m³/kg‐day (12.2) and m³/m²‐day (5.9). Higher absolute rates generally found in overweight/obese individuals compared to their normal‐weight counterparts suggest higher intakes of air pollutants (in μg/day) for the former compared to the latter during identical exposure concentrations and conditions. Highest absolute mean (24.57 m³/day) and 99th percentile (55.55 m³/day) values were found in obese class 2 adults. They inhale on average 8.21 m³ more air per day than normal‐weight adults.     

Bisphenol A: How the Most Relevant Exposure Sources Contribute to Total Consumer Exposure

Bisphenol A (BPA) is an endocrine disrupting chemical that is found in human urine throughout industrial societies around the globe. Consumer exposure pathways to BPA include packaged food, household dust, air, and dental fillings. To date, information on the relative contribution of the different pathways to total consumer exposure is lacking, but is key for managing substance‐associated risks. We investigated the relative contributions of the pathways known to be most relevant for nine different consumer groups. Our results suggest that the most important pathways for infants and children are the use of polycarbonate (PC) baby bottles and for adults and teenagers the consumption of canned food. Dental surgery can also considerably contribute over a short time directly after the surgery. For infants fed with PC baby bottles with mean dose rates of 0.8 μg/kg_bw/d the highest exposure dose rate was calculated. This dose rate is far below the tolerable daily intake of 50 μg/kg_bw/d. However, it is of the same order of magnitude as recently reported concentrations that caused low‐dose health effects in rodents. We find a pattern of falling exposure levels with rising age that is supported by urinary concentrations of BPA available for selected consumer groups. Similarly, the exposure levels we predict are confirmed by the levels reported in these studies.     

Cancer Dose-Response Modeling of Epidemiological Data on Worker Exposures to Aldrin and Dieldrin

The paper applies classical statistical principles to yield new tools for risk assessment and makes new use of epidemiological data for human risk assessment. An extensive clinical and epidemiological study of workers engaged in the manufacturing and formulation of aldrin and dieldrin provides occupational hygiene and biological monitoring data on individual exposures over the years of employment and provides unusually accurate measures of individual lifetime average daily doses. In the cancer dose-response modeling, each worker is treated as a separate experimental unit with his own unique dose. Maximum likelihood estimates of added cancer risk are calculated for multistage, multistage-Weibull, and proportional hazards models. Distributional characterizations of added cancer risk are based on bootstrap and relative likelihood techniques. The cancer mortality data on these male workers suggest that low-dose exposures to aldrin and dieldrin do not significantly increase human cancer risk and may even decrease the human hazard rate for all types of cancer combined at low doses (e.g., 1 g/kg/day). The apparent hormetic effect in the best fitting dose-response models for this data set is statistically significant. The decrease in cancer risk at low doses of aldrin and dieldrin is in sharp contrast to the U.S. Environmental Protection Agency's upper bound on cancer potency based on mouse liver tumors. The EPA's upper bound implies that lifetime average daily doses of 0.0000625 and 0.00625 g/kg body weight/day would correspond to increased cancer risks of 0.000001 and 0.0001, respectively. However, the best estimate from the Pernis epidemiological data is that there is no increase in cancer risk in these workers at these doses or even at doses as large as 2 g/kg/day.     

Assessing the Relationship Between Environmental Lead Concentrations and Adult Blood Lead Levels

This paper presents a model for predicting blood lead levels in adults who are exposed to elevated environmental levels of lead. The model assumes a baseline blood lead level based on average blood lead levels for adults described in two recent U.S. studies. The baseline blood lead level in adults arises primarily from exposure to lead in diet. Media-specific ingestion and absorption parameters are assessed for the adult population, and a biokinetic slope factor that relates uptake of lead into the body to blood lead levels is estimated. These parameters are applied to predict blood lead levels for adults exposed to a hypothetical site with elevated lead levels in soil, dust and air. Blood lead levels ranging from approximately 3-57 μg/dl are predicted, depending on the exposure scenarios and assumptions.     

Dose-Response Models for Inhalation of Bacillus anthracis Spores: Interspecies Comparisons

Because experiments with Bacillus anthracis are costly and dangerous, the scientific, public health, and engineering communities are served by thorough collation and analysis of experiments reported in the open literature. This study identifies available dose-response data from the open literature for inhalation exposure to B. anthracis and, via dose-response modeling, characterizes the response of nonhuman animal models to challenges. Two studies involving four data sets amenable to dose-response modeling were found in the literature: two data sets of response of guinea pigs to intranasal dosing with the Vollum and ATCC-6605 strains, one set of responses of rhesus monkeys to aerosol exposure to the Vollum strain, and one data set of guinea pig response to aerosol exposure to the Vollum strain. None of the data sets exhibited overdispersion and all but one were best fit by an exponential dose-response model. The beta-Poisson dose-response model provided the best fit to the remaining data set. As indicated in prior studies, the response to aerosol challenges is a strong function of aerosol diameter. For guinea pigs, the LD₅₀ increases with aerosol size for aerosols at and above 4.5 μm. For both rhesus monkeys and guinea pigs there is about a 15-fold increase in LD₅₀ when aerosol size is increased from 1 μm to 12 μm. Future experimental research and dose-response modeling should be performed to quantify differences in responses of subpopulations to B. anthracis and to generate data allowing development of interspecies correction factors.     

Duration Adjustment of Acute Exposure Guideline Level Values for Trichloroethylene Using a Physiologically-Based Pharmacokinetic Model

Acute Exposure Guideline Level (AEGL) recommendations are developed for 10-minute, 30-minute, 1-hour, 4-hours, and 8-hours exposure durations and are designated for three levels of severity: AEGL-1 represents concentrations above which acute exposures may cause noticeable discomfort including irritation; AEGL-2 represents concentrations above which acute exposure may cause irreversible health effects or impaired ability to escape; and AEGL-3 represents concentrations above which exposure may cause life-threatening health effects or death. The default procedure for setting AEGL values across durations when applicable data are unavailable involves estimation based on Haber's rule, which has an underlying assumption that cumulative exposure is the determinant of toxicity. For acute exposure to trichloroethylene (TCE), however, experimental data indicate that momentary tissue concentration, and not the cumulative amount of exposure, is important. We employed an alternative approach to duration adjustments in which a physiologically-based pharmacokinetic (PBPK) model was used to predict the arterial blood concentrations [TCE(a)] associated with adverse outcomes appropriate for AEGL-1, -2, or -3-level effects. The PBPK model was then used to estimate the atmospheric concentration that produces equivalent [TCE(a)] at each of the AEGL-specific exposure durations. This approach yielded [TCE(a)] values of 4.89 mg/l for AEGL-1, 18.7 mg/l for AEGL-2, and 310 mg/l for AEGL-3. Duration adjustments based on equivalent target tissue doses should provide similar degrees of toxicity protection at different exposure durations.     

Development of a Unit Risk Factor for 1,3-Butadiene Based on an Updated Carcinogenic Toxicity Assessment

The Texas Commission on Environmental Quality (TCEQ) has developed an inhalation unit risk factor (URF) for 1,3-butadiene based on leukemia mortality in an updated epidemiological study on styrene-butadiene rubber production workers conducted by researchers at the University of Alabama at Birmingham. Exposure estimates were updated and an exposure estimate validation study as well as dose-response modeling were conducted by these researchers. This information was not available to the U.S. Environmental Protection Agency when it prepared its health assessment of 1,3-butadiene in 2002. An extensive analysis conducted by TCEQ discusses dose-response modeling, estimating risk for the general population from occupational workers, estimating risk for potentially sensitive subpopulations, effect of occupational exposure estimation error, and use of mortality rates to predict incidence. The URF is 5.0 × 10⁻⁷ per μg/m³ or 1.1 × 10⁻⁶ per ppb and is based on a Cox regression dose-response model using restricted continuous data with age as a covariate, and a linear low-dose extrapolation default approach using the 95% lower confidence limit as the point of departure. Age-dependent adjustment factors were applied to account for possible increased susceptibility for early life exposure. The air concentration at 1 in 100,000 excess leukemia mortality, the no-significant-risk level, is 20 μg/m³ (9.1 ppb), which is slightly lower than the TCEQ chronic reference value of 33 μg/m³ (15 ppb) protective of ovarian atrophy. These values will be used to evaluate ambient air monitoring data so the general public is protected against adverse health effects from chronic exposure to 1,3-butadiene.     

Potential Exposure and Cancer Risk from Formaldehyde Emissions from Installed Chinese Manufactured Laminate Flooring

Lumber Liquidators (LL) Chinese‐manufactured laminate flooring (CLF) has been installed in >400,000 U.S. homes over the last decade. To characterize potential associated formaldehyde exposures and cancer risks, chamber emissions data were collected from 399 new LL CLF, and from LL CLF installed in 899 homes in which measured aggregate indoor formaldehyde concentrations exceeded 100 μg/m³ from a total of 17,867 homes screened. Data from both sources were combined to characterize LL CLF flooring‐associated formaldehyde emissions from new boards and installed boards. New flooring had an average (±SD ) emission rate of 61.3 ± 52.1 μg/m²‐hour; >one‐year installed boards had ∼threefold lower emission rates. Estimated emission rates for the 899 homes and corresponding data from questionnaires were used as inputs to a single‐compartment, steady‐state mass‐balance model to estimate corresponding residence‐specific TWA formaldehyde concentrations and potential resident exposures. Only ∼0.7% of those homes had estimated acute formaldehyde concentrations >100 μg/m³ immediately after LL CLF installation. The TWA daily formaldehyde inhalation exposure within the 899 homes was estimated to be 17 μg/day using California Proposition 65 default methods to extrapolate cancer risk (below the regulation “no significant risk level” of 40 μg/day). Using a U.S. Environmental Protection Agency linear cancer risk model, 50th and 95th percentile values of expected lifetime cancer risk for residents of these homes were estimated to be 0.33 and 1.2 per 100,000 exposed, respectively. Based on more recent data and verified nonlinear cancer risk assessment models, LL CLF formaldehyde emissions pose virtually no cancer risk to affected consumers.     

A dose-response analysis of skin cancer from inorganic arsenic in drinking water

A study of the prevalence of skin cancer among 40,421 persons consuming arsenic-contaminated drinking water in Taiwan was used for a cancer dose-response assessment of ingested arsenic. The numbers of persons at risk over three dose intervals and four exposure durations were estimated from the data in order to apply the method of maximum likelihood to a multistage-Weibull time/dose-response model. A constant exposure level since birth for each of the exposure categories was assumed. It was found that the cumulative hazard increases as a power of three in age, and is linear or quadratic (with a linear coefficient) in dose. Observations from a smaller epidemiologic survey in Mexico were similar to what would be predicted from the model of the Taiwan data. Assuming that the skin cancer risk from ingested arsenic in the American population would also be similar to the Taiwan population, an American male would have a lifetime risk of developing skin cancer of 1.3 x 10(-3) (3.0 x 10(-3] if exposed to 1 microgram/kg/day for a 76-year lifespan (median lifespan in the U.S.).     

Health Risk Assessment of a Modern Municipal Waste Incinerator

During the modernization of the municipal waste incinerator (MWI, maximum capacity of 180,000 tons per year) of Metropolitan Grenoble (405,000 inhabitants), in France, a risk assessment was conducted, based on four tracer pollutants: two volatile organic compounds (benzene and 1, 1, 1 trichloroethane) and two heavy metals (nickel and cadmium, measured in particles). A Gaussian plume dispersion model, applied to maximum emissions measured at the MWI stacks, was used to estimate the distribution of these pollutants in the atmosphere throughout the metropolitan area. A random sample telephone survey (570 subjects) gathered data on time-activity patterns, according to demographic characteristics of the population. Life-long exposure was assessed as a time-weighted average of ambient air concentrations. Inhalation alone was considered because, in the Grenoble urban setting, other routes of exposure are not likely. A Monte Carlo simulation was used to describe probability distributions of exposures and risks. The median of the life-long personal exposures distribution to MWI benzene was 3.2·10^–5 g/m³ (20th and 80th percentiles = 1.5·10^–5 and 6.5·10^–5 g/m³), yielding a 2.6·10^–10 carcinogenic risk (1.2·10^–10–5.4·10^–10). For nickel, the corresponding life-time exposure and cancer risk were 1.8·10^–4 g/m³ (0.9.10^–4 – 3.6·10^–4 g/m³) and 8.6·10^–8 (4.3·10^–8–17.3·10^–8); for cadmium they were respectively 8.3·10^–6 g/m³ (4.0·10^–6–17.6·10^–6) and 1.5·10^–8 (7.2·10^–9–3.1·10^–8). Inhalation exposure to cadmium emitted by the MWI represented less than 1% of the WHO Air Quality Guideline (5 ng/m³), while there was a margin of exposure of more than 10⁹ between the NOAEL (150 ppm) and exposure estimates to trichloroethane. Neither dioxins nor mercury, a volatile metal, were measured. This could lessen the attributable life-long risks estimated. The minute (VOCs and cadmium) to moderate (nickel) exposure and risk estimates are in accord with other studies on modern MWIs meeting recent emission regulations, however.