Segregation and black/white differences in exposure to air toxics in 1990

I examined non-Hispanic Black and non-Hispanic White differences in exposure to noncriteria air pollutants in 44 U.S. Census Bureau-defined metropolitan areas with populations greater than one million, using data on air toxics concentrations prepared for the U.S. Environmental Protection Agency as part of its Cumulative Exposure Project combined with U.S. census data. I measured differences in exposure to air toxics through the calculation of a net difference score, which is a statistical measure used in income inequality analysis to measure inequality over the whole range of exposures. The scores ranged from 11.52 to 83.60. In every metropolitan area, non-Hispanic Blacks are more likely than non-Hispanic Whites to be living in tracts with higher total modeled air toxics concentrations. To assess potential reasons for such a wide variation in exposure differences, I performed a multiple regression analysis with the net difference score as the dependent variable. Independent variables initially included were as follows: the dissimilarity index (to measure segregation), Black poverty/White poverty (to control for Black/White economic differences), population density and percentage of persons traveling to work who drive to work (alone and in car pools), and percentage of workforce employed in manufacturing (factors affecting air quality). After an initial analysis I eliminated from the model the measures of density and the persons driving to work because they were statistically insignificant, they did not add to the predictive power of the model, and their deletion did not affect the other variables. The final model had an R(2) of 0.56. Increased segregation is associated with increased disparity in potential exposure to air pollution.     

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.     

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.     

Personal exposure monitoring of particulate matter,nitrogen dioxide,and carbon monoxide,including susceptible groups

Aims: To investigate the relation between personal exposures to nitrogen dioxide, carbon monoxide, and PM₁₀, and exposures estimated from static concentrations of these pollutants measured within the same microenvironments, for healthy individuals and members of susceptible groups.     

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.     

Geographic boundaries in breast,lung and colorectal cancers in relation to exposure to air toxics in Long Island,New York

Background  

This two-part study employs several statistical techniques to evaluate the geographic distribution of breast cancer in females and colorectal and lung cancers in males and females in Nassau, Queens, and Suffolk counties, New York, USA. In this second paper, we compare patterns in standardized morbidity ratios (SMR values), calculated from New York State Department of Health (NYSDOH) data, to geographic patterns in overall predicted risk (OPR) from air toxics using exposures estimated in the USEPA National Air Toxics Assessment database.     

Respirator use and protection from exposure to carbon monoxide

Investigations of the protective effect afforded by respirators in Baltimore firefighters are presented. The data indicates that the continuous use of respirators offers significant protection from exposure to carbon monoxide but that this protection is not absolute. A surprising finding is that the intermittent use of the face mask offers as little protection to the men as does non-use. These findings emphasize the difficulties in relying upon respiratory personal protective equipment for protection from exposure.     

Expired air carbon monoxide and serum thiocyanate as objective measures of cigarette exposure.

Expired air carbon monoxide (CO) and serum thiocyanate (SCN) were used to asses exposure to cigarettes in 139 middle-aged men. Subjects who reported smoking cigarettes generally had CO levels exceeding 8ppm and SCN levels exceeding 100umol/L; non-smokers had lower levels. For both tests the mean concentration among men smoking more than one pack daily was three times that of non-smokers. The is a high correlation between the two tests (r=.571 for smokers), an association that was largely independent of the smaller correlations between either test and reported smoking frequency (r=.476 for CO; r=.479 for SCN). The ability to distinguish between individuals who reported "typical" smoking habits and non-smokers was best when the CO and SCN analyses were used together to take advantage of their separate sources of variance; it was 99 per cent when the two tests were mutually concordant (91 per cent of cases). The CO and SCN measurements allowed 16 individuals who reported light smoking habits to be categorized into high and low presumptive tobacco exposure groups. The two tests are inexpensive and suitable for use in epidemiologic and health care delivery programs.     

Formation of carbon monoxide in air compressors.

Oil-lubricated compressors are said to contaminate the air they compress with carbon monixde from pyrolyzed and oxidized lubricants. Experiments were performed in an instrumented compressor to determine if synthetic oils as lubricants would results in less contamination. The results suggest that for all oils the contamination is actually not great. Published results from low-temperature oxidation of hydrocarbons support this estimate.     

Evaluation of exposure to carbon monoxide associated with passive smoking

The current study measured breath carbon monoxide (CO) concentrations prior to and at prescribed time intervals after exposure to passive smoking under controlled conditions, along with the air CO concentration in the exposure room during the exposure periods. The postexposure breath CO levels were 1.4-2.7 times higher than the background breath CO levels after 30 min of exposure, yet only slightly higher after 10 min of exposure, thereby confirming that exposure to CO from passive smoking causes a significant body burden of CO. The air CO concentration gradually increased during the burning of a cigarette(s), regardless of the exposure duration, whereas it slightly decreased after burning. However, the pattern of breath CO decay was similar for the two different types of exposure (during and after a cigarette(s)) in each subject. The decrease in the postexposure alveolar CO concentrations was slow even in the early phase of the decay curves, indicating a monocompartment uptake and elimination model for the human body. The half-lives (78-277 min) estimated in the present study were comparable to those reported in previous studies associated with CO exposure from active smoking or other activities. The current study also evaluated the CO exposure of visitors and workers at three different types of recreation facility (bars, Internet cafes, and billiard halls) typically associated with passive smoking. The results confirmed that passive smoking is the major contributor to the CO exposure of nonsmoking visitors in a recreation environment. In addition, workplace exposure to CO from passive smoking was found to be the most important contributor to the daily CO exposure of nonsmoking recreation workers.     

Cardiovascular adjustments to carbon monoxide exposure during rest and exercise in dogs

Cardiovascular, respiratory, and metabolic measurements were made on dogs at rest and during 30 minutes of exercise at either 6.4 km/hour, 10% grade, or 8.0 km/hour, 16% grade, following the bolus administration of CO for 1 or 2 minutes, or room-air breathing mixtures. During rest and exercise elevated mean blood HbCO levels (6 to 21%) reduced the arterial and mixed venous oxygen contents and saturations, and mixed venous P_O2 levels. Arterial-mixed venous oxygen differences were reduced during exercise as a result of CO administration. Elevated blood HbCO levels had a minimal or no effect on other cardiovascular, respiratory, and metabolic parameters. During work the reductions in a-v?_O2 differences were not offset by appropriate increases in cardiac outputs.