Risk assessment and risk management of noncriteria pollutants.

Noncriteria air pollutants are synonymous with hazardous air pollutants (HAPs), air toxics or toxic air pollutants (TAPs). The term noncriteria pollutants refers to all air pollutants except for the criteria pollutants (SOx, PM, NOx, CO, O3, and Pb). Air toxics are pervasive in our environment worldwide in varying degrees. Uses of these chemicals are varied and numerous; their emissions are ubiquitous, and they include organic compounds such as chlorinated hydrocarbons, dioxins, aldehydes, polynuclear aromatic hydrocarbons, and heavy metals such as chromium, nickel, cadmium, and mercury. There are more than 70,000 chemicals that are in use commercially in the United States, and we know relatively little about their ambient concentrations, persistence, transport and transformation as well as their effects on health and the environment, many of which take decades to emerge. The United States Environmental Protection Agency, under the authority of Section 112 of the Clean Air Act, is mandated to regulate any air pollutant which, in the Administrator's judgment, "causes, or contributes to, air pollution which may reasonably be anticipated to result in an increase in serious irreversible or incapacitating reversible illness." For such regulatory decision-making, EPA's Office of Health and Environmental Assessment (OHEA) provides scientific assessment of health effects for potentially hazardous air pollutants. In accordance with risk assessment guidelines developed by OHEA over the years, Health Assessment Documents (HADs) containing risk assessment information were prepared and were subjected to critical review and careful revision to produce Final Draft HADs which serve as scientific databases for regulatory decision-making by the Office of Air Quality Planning and Standards (OAQPS) in its risk management process. EPA developed databases such as the Integrated Risk Information System (IRIS) and the National Air Toxics Information Clearinghouse (NATICH) and a technical assistance response system called the Air Risk Information Support Center (AIR RISC), in addition, to help in implementation of the National Air Toxics Program by state and local regulators.     

Implications of OSHA's reliance on TLVs in developing the air contaminants standard

This paper evaluates the decision by the Occupational Safety and Health Administration (OSHA) to base its Air Contaminants Standard on the threshold limit values (TLVs) of the American Conference of Governmental Industrial Hygienists. Contrary to the claim made by OSHA in promulgating the standard, the TLV list was not the sole available basis for a generic standard covering toxic air contaminants. The National Institute for Occupational Safety and Health (NIOSH) presented data indicating that the TLVs were insufficiently protective for 98 substances. NIOSH Recommended Exposure Limits (RELs) were available for 59 of these substances. The ratio of PEL to REL ranged up to 1,000, with a median of 2.5 and a mean of 71.4. OSHA excluded 42 substances from the standard altogether despite the availability of NIOSH RELs, solely because no TLV had been established.     

Assessing exposure to air toxics relative to asthma

Asthma is a respiratory disease whose prevalence has been increasing since the mid 1970s and that affects more than 14.6 million residents of the United States. Environmental triggers of asthma include air pollutants that are respiratory irritants. Air toxics emitted into the ambient air are listed in the 1990 Clean Air Act Amendments as hazardous air pollutants (HAPs) if they can adversely affect human health, including the respiratory tract. HAPs include particulate and gaseous-phase pollutants, individual organic compounds and metals, and mixtures. Associations between asthma exacerbation and both particles and indoor volatile organic compounds (VOCs), often referred to as indoor air quality, have been reported. Studies conducted in the United States, Canada, and Europe over the past two decades have shown that most people living in the developed countries spend the majority of their time indoors and that the air concentrations of many air toxics or HAPs are higher indoors than in the ambient air in urban, suburban, and rural settings. Elevated indoor air concentrations result from emissions of air toxics from consumer products, household furnishings, and personal activities. The Relationship of Indoor, Outdoor and Personal Air (RIOPA) study was designed to oversample homes in close proximity to ambient sources, excluding residences where smokers lived, to determine the contribution of ambient emissions to air toxics exposure. The ratios of indoor to outdoor air concentrations of some VOCs in homes measured during RIOPA were much greater than one, and for most other VOCs that had indoor-to-outdoor ratios close to unity in the majority of homes, elevated ratios were found in the paired samples with the highest concentration. Thus, although ambient emissions contribute to exposure of some air toxics indoors as well as outdoors, this was not true for all of the air toxics and especially for the higher end of exposures to most volatile organic air toxics examined. It is therefore critical, when evaluating potential effects of air toxics on asthma or other adverse health end points, to determine where the exposure occurs and the source contributions for each air toxic and target population separately and not to rely solely on ambient air concentration measurements.     

Separate and unequal: residential segregation and estimated cancer risks associated with ambient air toxics in U.S. metropolitan areas

This study examines links between racial residential segregation and estimated ambient air toxics exposures and their associated cancer risks using modeled concentration estimates from the U.S. Environmental Protection Agency's National Air Toxics Assessment. We combined pollutant concentration estimates with potencies to calculate cancer risks by census tract for 309 metropolitan areas in the United States. This information was combined with socioeconomic status (SES) measures from the 1990 Census. Estimated cancer risks associated with ambient air toxics were highest in tracts located in metropolitan areas that were highly segregated. Disparities between racial/ethnic groups were also wider in more segregated metropolitan areas. Multivariate modeling showed that, after controlling for tract-level SES measures, increasing segregation amplified the cancer risks associated with ambient air toxics for all racial groups combined [highly segregated areas: relative cancer risk (RCR) = 1.04; 95% confidence interval (CI), 1.01-107; extremely segregated areas: RCR = 1.32; 95% CI, 1.28-1.36]. This segregation effect was strongest for Hispanics (highly segregated areas: RCR = 1.09; 95% CI, 1.01-1.17; extremely segregated areas: RCR = 1.74; 95% CI, 1.61-1.88) and weaker among whites (highly segregated areas: RCR = 1.04; 95% CI, 1.01-1.08; extremely segregated areas: RCR = 1.28; 95% CI, 1.24-1.33), African Americans (highly segregated areas: RCR = 1.09; 95% CI, 0.98-1.21; extremely segregated areas: RCR = 1.38; 95% CI, 1.24-1.53), and Asians (highly segregated areas: RCR = 1.10; 95% CI, 0.97-1.24; extremely segregated areas: RCR = 1.32; 95% CI, 1.16-1.51). Results suggest that disparities associated with ambient air toxics are affected by segregation and that these exposures may have health significance for populations across racial lines.     

The impact of a change to inhalable occupational exposure limits: strontium chromate exposure in the U.S. Air Force

The American Conference of Governmental Industrial Hygienists has announced its intention to replace all total particulate threshold limit values (TLVs) with size-selective TLVs. Because the U.S. Air Force has adopted the TLVs as its occupational exposure limits, the impact of this change is of interest, specifically for hexavalent chromium. This article reviews historical strontium chromate sampling data in the Air Force and the impact of its reinterpretation in comparison to an inhalable TLV. Based on the measured conversion factor between the 37-mm cassette and the IOM inhalable sampler, inhalable strontium chromate exposures will continue to exceed the TLV during all aircraft priming and most sanding procedures. In addition, inhalable exposures are expected to exceed 1000 times the TLV, greater than the highest currently assigned protection factor for airline respirators, during 25% of priming procedures. Without a change in the value of the current TLV time-weighted average of 0.5 microg/m(3), the Air Force will need to reduce strontium chromate levels, either by incorporating work practices that decrease worker productivity or considering a change to nonchromated primers.     

Assessing the health implications for healthcare workers of regulatory changes eliminating locally developed occupational exposure limits in favor of TLVs: an evidence-based bipartite approach

In response to the intention of the Workers' Compensation Board of British Columbia (WCB of BC) to eliminate made-in-BC occupational exposure limits (OELs) and adopt threshold limit values (TLVs), this study assessed the potential health impacts on healthcare workers (HCWs) of the proposed change, by (1) reviewing the processes used to establish the OELs and TLVs, (2) selecting of substances of health concern for HCWs, (3) identifying chemicals with discordances between existing OELs and the 2002 TLVs, and 4) reviewing the discordances and assessing the potential health implications. Differences in philosophies, policies and processes that influenced the setting of OELs and TLVs were substantial. The TLV process involves U.S. and international priorities; in BC, a tripartite committee determined OELs taking into consideration how OELs should be interpreted in the local context. 47 chemicals of concern to BC HCWs were discordant, with significant discordances totalling 57; 15 compounds had BC 8-hour OELs lower than their respective TLVs and three TLVs were lower than the 8-hour BC OELs. Review of six chemicals with discordances suggested a potential for increased risks of adverse health effects. Eliminating the local capacity and authority to set OELs is unlikely to cause major health problems in the short run, but as chemicals in use locally may not have up-to-date TLVs, eliminating the capacity for local considerations should be undertaken with great caution. While the WCB of BC did implement the change, the present report resulted in procedural changes that will provide better protection for the workforce.     

Inhalation exposure and risk from mobile source air toxics in future years

Modeling of inhalation exposure and risks resulting from exposure to mobile source air toxics can be used to evaluate impacts of reductions from control programs on overall risk, as well as changes in relative contributions of different source sectors to risk, changes in contributions of different pollutants to overall risk, and changes in geographic distributions of risk. Such analysis is useful in setting regulatory priorities, and informing the decision-making process. In this paper, we have conducted national-scale air quality, exposure, and risk modeling for the US in the years 2015, 2020, and 2030, using similar tools and methods as the 1999 National-Scale Air Toxics Assessment. Our results suggest that US Environmental Protection Agency emission control programs will substantially reduce average inhalation cancer risks and potential noncancer health risks from exposure to mobile source air toxics. However, cancer risk and noncancer hazard due to inhalation of air toxics will continue to be a public health concern.     

An assessment of air toxics in Minnesota

We used monitoring and modeling to assess the concentrations of air toxics in the state of Minnesota. Model-predicted concentrations for 148 hazardous air pollutants were from the U.S. Environmental Protection Agency Cumulative Exposure Project (1990 data). Monitoring data consisted of samples of volatile organic compounds, carbonyls, and particulate matter [Less than and equal to] 10 microm in aerodynamic diameter collected at 25 sites throughout the state for varying periods of time (up to 8 years; 1991-1998). Ten pollutants exceeded health benchmark values at one or more sites by modeling, monitoring, or both (including acrolein, arsenic, benzene, 1,3-butadiene, carbon tetrachloride, chromium, chloroform, ethylene dibromide, formaldehyde, and nickel). Polycyclic organic matter also exceeded the benzo[a]pyrene health benchmark value assumed to represent this class of pollutants. The highest modeled and monitored concentrations of most pollutants were near the center of the Minneapolis-St. Paul metropolitan area; however, many smaller cities throughout the state also had elevated concentrations. Where direct comparisons were possible, monitored values often tended to exceed model estimates. Upper-bound excess lifetime inhalation cancer risks were estimated to range from 2.7 [times] 10(-5) to 140. 9 [times] 10(-5) (modeling) and 4.7 [times] 10(-5) to 11.0 [times] 10(-5) (using a smaller set of monitored carcinogens). Screening noncancer hazard indices summed over all end points ranged from 0.2 to 58.1 (modeling) and 0.6 to 2.0 (with a smaller set of monitored pollutants). For common sets of pollutants, the concentrations, cancer risks, and noncancer hazard indices were comparable between model-based estimates and monitored values. The inhalation cancer risk was apportioned to mobile sources (54%), area sources (22%), point sources (12%), and background (12%). This study provides evidence that air toxics are a public health concern in Minnesota.     

Estimating risk from ambient concentrations of acrolein across the United States

BACKGROUND: Estimated ambient concentrations of acrolein, a hazardous air pollutant, are greater than the U.S. Environmental Protection Agency (EPA) reference concentration throughout the United States, making it a concern for human health. However, there is no method for assessing the extent of risk under the U.S. EPA noncancer risk assessment framework. OBJECTIVES: We estimated excess risks from ambient concentrations of acrolein based on dose-response modeling of a study in rats with a relationship between acrolein and residual volume/total lung capacity ratio (RV/TLC) and specific compliance (sC(L)), markers for altered lung function. METHODS: Based on existing literature, we defined values above the 90th percentile for controls as "adverse." We estimated the increase over baseline response that would occur in the human population from estimated ambient concentrations of acrolein, taken from the U.S. EPA's National-Scale Air Toxics Assessment for 1999, after standard animal-to-human conversions and extrapolating to doses below the experimental data. RESULTS: The estimated median additional number of adverse sC(L) outcomes across the United States was approximately 2.5 cases per 1,000 people. The estimated range of additional outcomes from the 5th to the 95th percentile of acrolein concentration levels across census tracts was 0.28-14 cases per 1,000. For RV/TLC, the median additional outcome was 0.002 per 1,000, and the additional outcome at the 95th percentile was 0.13 per 1,000. CONCLUSIONS: Although there are uncertainties in estimating human risks from animal data, this analysis demonstrates a method for estimating health risks for noncancer effects and suggests that acrolein could be associated with decreased respiratory function in the United States.     

Air contaminant exposures during the operation of lawn and garden equipment

The US Environmental Protection Agency (EPA) initiated the Small Engine Exposure Study (SEES) to evaluate potential exposures among users of small, gasoline-powered, non-road spark-ignition (SI) lawn and garden engines. Equipment tested included riding tractors, walk-behind lawn mowers, string trimmers, and chainsaws. Personal and background air quality measurements were collected on equipment operators for carbon monoxide (CO), particulate matter 相似文献   

Air toxics in the U.S.: magnitude of the problem and strategy for control

Over the past several years, substantial concern has been expressed by some in Congress, environmental groups, and members of the public concerning the lack of progress in regulating toxic air pollutants by the U.S. Environmental Protection Agency (EPA). As a result, a number of amendments to the Federal Clean Air Act have been introduced to require EPA to regulate in a relatively rapid timeframe, a large number of potentially toxic pollutants that are released to the ambient air. This paper discusses EPA's current understanding of the magnitude and nature of the air toxics problem in the U.S., and the pollutants and source categories that pose the most significant risk to the public. The focus of the discussion is on routine releases, as opposed to catastrophic, accidental releases such as the one in Bhopal, India. The paper then discusses the strategy that EPA has put in place to deal with the problem and presents the status of a number of regulatory and non-regulatory activities under way to better understand the problem and to mitigate it. The strategy involves important roles for: (1) EPA to regulate national problems using a variety of Federal authorities in addition to the Clean Air Act, and (2) States to develop their own air toxic control programs to deal with unique local problems involving high risk point sources and multipollutant, multisource problems in large urban or industrialized areas.     

Workers’ exposures and potential health risks to air toxics in a petrochemical complex assessed by improved methodology

Objective This study was designed to comprehensively evaluate workers’ potential health risks of exposure to 39 air toxics in the Ta-sher Petrochemical Complex. Methods: Open-Path Fourier Transform Infrared Spectroscopy (OP-FTIR) was used to measure concentrations of air toxics. We used the measured worksite concentrations between 1997 and 1999 at 11 companies in the petrochemical complex, employing 3,100 on-site workers. The 39 measured air toxics included 10 chemicals with acute reference exposure levels (RELa), 19 chemicals with chronic reference exposure levels (RELc), and 3 chemicals classified as Class 1 or 2A human carcinogens by the International Agency for Research on Cancer (IARC). We then used RELa to calculate the hazard index of acute health effects (HI _A ) for workers in individual plants. We also calculated the hazard index of chronic health effects (HIc) and cancer risks for all workers in the entire petrochemical complex. Results: Workers in five companies had HI _A greater than 1 because of toluene, benzene, methyl ethyl ketone, chloroform and isopropanol exposures. Workers in this petrochemical complex had HIc greater than 1 because of acrylonitrile, 1,3-butadiene, hydrogen cyanide, and n,n-dimethylformamide exposures. Risk of hematopoietic system cancer because of benzene and ethylene oxide exposure, and respiratory system cancer because of 1,3-butadiene exposure was estimated to be 3.1–6.1×10⁻⁴ and 5.2–7.1×10⁻⁴, respectively. Conclusions: Our findings indicated that workers in the petrochemical complex might have excess cancer and noncancer risks due to acute or chronic exposures to air toxics from multiple emission sources.     

EPA's control technology approach to assisting states and regions with air toxics problems: five case studies

The Environmental Protection Agency (EPA) announced in June 1985 a new strategy to reduce public exposure to toxic air pollutants in the ambient air. Over the next 5-8 years, the strategy called for State and Local authorities to take on more of the lead regulatory role, with the Agency providing technical and financial assistance to their efforts. The shift in emphasis and responsibility from the Federal level to State and Local air toxics programs and the need to transfer expertise from the Federal level to the appropriate State or Local level prompted EPA's Office of Research and Development (ORD) and EPA's Office of Air Quality Planning and Standards (OAQPS) to develop and implement an innovative technical assistance program. This program is called the Control Technology Center (CTC). It has since been expanded to include technical assistance in the area of control of air toxics, particulate matter, and volatile organic compounds (VOCs); emission measurements; and other areas where expertise is available to ORD and OAQPS. During the CTC's first year of operation, operating guidelines were developed and three categories of technical assistance were established. These categories are telephone HOTLINE calls, direct engineering assistance, and technical guidance projects. The CTC HOTLINE is a special telephone number which State and Local Agencies can call for easy access to EPA personnel who can provide prompt assistance in a variety of ways including discussions, references to pertinent literature, and referrals to other EPA personnel. In some cases, a HOTLINE call will require more in-depth engineering analysis indicating a need for direct engineering assistance. These projects tend to be short-term (2 to 3 months) and specific in nature. In some cases, several agencies may indicate a need for information on the same source, or a group of Agencies may make a joint request. In these cases, the CTC Steering Committee, a group who advises the CTC managers, may decide that a technical guidance project is indicated. Technical guidance projects are longer-term and are intended to be of broad interest, useful to many agencies. This paper discusses the development of the CTC, experience to date with its operation, and future plans. In addition, five CTC projects are discussed to illustrate the assistance provided.     

Meeting report: Estimating the benefits of reducing hazardous air pollutants--summary of 2009 workshop and future considerations

Background

Quantifying the benefits of reducing hazardous air pollutants (HAPs, or air toxics) has been limited by gaps in toxicological data, uncertainties in extrapolating results from high-dose animal experiments to estimate human effects at lower doses, limited ambient and personal exposure monitoring data, and insufficient economic research to support valuation of the health impacts often associated with exposure to individual air toxics.

Objectives

To address some of these issues, the U.S. Environmental Protection Agency held the Workshop on Estimating the Benefits of Reducing Hazardous Air Pollutants (HAPs) in Washington, DC, from 30 April to 1 May 2009.

Discussion

Experts from multiple disciplines discussed how best to move forward on air toxics benefits assessment, with a focus on developing near-term capability to conduct quantitative benefits assessment. Proposed methodologies involved analysis of data-rich pollutants and application of this analysis to other pollutants, using dose–response modeling of animal data for estimating benefits to humans, determining dose-equivalence relationships for different chemicals with similar health effects, and analysis similar to that used for criteria pollutants. Limitations and uncertainties in economic valuation of benefits assessment for HAPS were discussed as well.

Conclusions

These discussions highlighted the complexities in estimating the benefits of reducing air toxics, and participants agreed that alternative methods for benefits assessment of HAPs are needed. Recommendations included clearly defining the key priorities of the Clean Air Act air toxics program to identify the most effective approaches for HAPs benefits analysis, focusing on susceptible and vulnerable populations, and improving dose–response estimation for quantification of benefits.     

Exposures to multiple air toxics in New York City

Efforts to assess health risks associated with exposures to multiple urban air toxics have been hampered by the lack of exposure data for people living in urban areas. The TEACH (Toxic Exposure Assessment, a Columbia/Harvard) study was designed to characterize levels of and factors influencing personal exposures to urban air toxics among high school students living in inner-city neighborhoods of New York City and Los Angeles, California. This present article reports methods and data for the New York City phase of TEACH, focusing on the relationships between personal, indoor, and outdoor concentrations in winter and summer among a group of 46 high school students from the A. Philip Randolph Academy, a public high school located in the West Central Harlem section of New York City. Air pollutants monitored included a suite of 17 volatile organic compounds (VOCs) and aldehydes, particulate matter with a mass median aerodynamic diameter 相似文献   

Distributional benefit analysis of a national air quality rule

Under Executive Order 12898, the U.S. Environmental Protection Agency (EPA) must perform environmental justice (EJ) reviews of its rules and regulations. EJ analyses address the hypothesis that environmental disamenities are experienced disproportionately by poor and/or minority subgroups. Such analyses typically use communities as the unit of analysis. While community-based approaches make sense when considering where polluting sources locate, they are less appropriate for national air quality rules affecting many sources and pollutants that can travel thousands of miles. We compare exposures and health risks of EJ-identified individuals rather than communities to analyze EPA's Heavy Duty Diesel (HDD) rule as an example national air quality rule. Air pollutant exposures are estimated within grid cells by air quality models; all individuals in the same grid cell are assigned the same exposure. Using an inequality index, we find that inequality within racial/ethnic subgroups far outweighs inequality between them. We find, moreover, that the HDD rule leaves between-subgroup inequality essentially unchanged. Changes in health risks depend also on subgroups' baseline incidence rates, which differ across subgroups. Thus, health risk reductions may not follow the same pattern as reductions in exposure. These results are likely representative of other national air quality rules as well.     

火焰原子吸收法测定工作场所空气中氧化镁方法验证实验研究

目的为了验证工作场所空气中氧化镁测定的标准方法在作者所在实验室的适应性,确保该检测方法的检测质量。方法按照国家职业卫生标准《工作场所空气有毒物质镁及其化合物》(GBZ/T 160.12—2004)[1]规定,绘制镁标准曲线,对模拟滤膜做加标回收试验、精密度测定试验、检出限测定。结果镁标准曲线相关系数r=1.000,加标回收率为95.5%～97.0%,精密度RSD为0.96%～2.8%,方法检出限为:6.1×10-3μg/ml。结论该实验室实验条件和测试结果均能满足国家标准的要求,该实验室可以使用国家职业卫生标准《工作场所空气有毒物质镁及其化合物》开展氧化镁的检测工作。     

Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational,indoor, and community air pollution research

Outdoor ambient air pollutant exposures in communities are relevant to the acute exacerbation and possibly the onset of asthma. However, the complexity of pollutant mixtures and etiologic heterogeneity of asthma has made it difficult to identify causal components in those mixtures. Occupational exposures associated with asthma may yield clues to causal components in ambient air pollution because such exposures are often identifiable as single-chemical agents (e.g., metal compounds). However, translating occupational to community exposure-response relationships is limited. Of the air toxics found to cause occupational asthma, only formaldehyde has been frequently investigated in epidemiologic studies of allergic respiratory responses to indoor air, where general consistency can be shown despite lower ambient exposures. The specific volatile organic compounds (VOCs) identified in association with occupational asthma are generally not the same as those in studies showing respiratory effects of VOC mixtures on nonoccupational adult and pediatric asthma. In addition, experimental evidence indicates that airborne polycyclic aromatic hydrocarbon (PAH) exposures linked to diesel exhaust particles (DEPs) have proinflammatory effects on airways, but there is insufficient supporting evidence from the occupational literature of effects of DEPs on asthma or lung function. In contrast, nonoccupational epidemiologic studies have frequently shown associations between allergic responses or asthma with exposures to ambient air pollutant mixtures with PAH components, including black smoke, high home or school traffic density (particularly truck traffic), and environmental tobacco smoke. Other particle-phase and gaseous co-pollutants are likely causal in these associations as well. Epidemiologic research on the relationship of both asthma onset and exacerbation to air pollution is needed to disentangle effects of air toxics from monitored criteria air pollutants such as particle mass. Community studies should focus on air toxics expected to have adverse respiratory effects based on biological mechanisms, particularly irritant and immunological pathways to asthma onset and exacerbation.     

Risk of leukemia in relation to exposure to ambient air toxics in pregnancy and early childhood

There are few established causes of leukemia, the most common type of cancer in children. Studies in adults suggest a role for specific environmental agents, but little is known about any effect from exposures in pregnancy to toxics in ambient air. In our case–control study, we ascertained 69 cases of acute lymphoblastic leukemia (ALL) and 46 cases of acute myeloid leukemia (AML) from California Cancer Registry records of children <age 6, and 19,209 controls from California birth records within 2 km (1.3 miles) (ALL) and 6 km (3.8 miles) (AML) of an air toxics monitoring station between 1990 and 2007. Information on air toxics exposures was taken from community air monitors. We used logistic regression to estimate the risk of leukemia associated with one interquartile range increase in air toxic exposure. Risk of ALL was elevated with 3^rd trimester exposure to polycyclic aromatic hydrocarbons (OR = 1.16, 95% CI 1.04, 1.29), arsenic (OR = 1.33, 95% CI 1.02, 1.73), benzene (OR = 1.50, 95% CI 1.08, 2.09), and three other toxics related to fuel combustion. Risk of AML was increased with 3rd trimester exposure to chloroform (OR = 1.30, 95% CI 1.00, 1.69), benzene (1.75, 95% CI 1.04, 2.93), and two other traffic-related toxics. During the child's first year, exposure to butadiene, ortho-xylene, and toluene increased risk for AML and exposure to selenium increased risk for ALL. Benzene is an established cause of leukemia in adults; this study supports that ambient exposures to this and other chemicals in pregnancy and early life may also increase leukemia risk in children.