Potential for Electric Vehicle Adoption to Mitigate Extreme Air Quality Events in China.

Electric vehicle (EV) adoption promises potential air pollutant and greenhouse gas (GHG) reduction co-benefits. As such, China has aggressively incentivized EV adoption, however much remains unknown with regard to EVs' mitigation potential, including optimal vehicle type prioritization, power generation contingencies, effects of Clean Air regulations, and the ability of EVs to reduce acute impacts of extreme air quality events. Here, we present a suite of scenarios with a chemistry transport model that assess the potential co-benefits of EVs during an extreme winter air quality event. We find that regardless of power generation source, heavy-duty vehicle (HDV) electrification consistently improves air quality in terms of NO2 and fine particulate matter (PM2.5), potentially avoiding 562 deaths due to acute pollutant exposure during the infamous January 2013 pollution episode (~1% of total premature mortality). However, HDV electrification does not reduce GHG emissions without enhanced emission-free electricity generation. In contrast, due to differing emission profiles, light-duty vehicle (LDV) electrification in China consistently reduces GHG emissions (~2 Mt CO2), but results in fewer air quality and human health improvements (145 avoided deaths). The calculated economic impacts for human health endpoints and CO2 reductions for LDV electrification are nearly double those of HDV electrification in present-day (155M vs. 87M US$), but are within ~25% when enhanced emission-free generation is used to power them. Overall, we find only a modest benefit for EVs to ameliorate severe wintertime pollution events, and that continued emission reductions in the power generation sector will have the greatest human health and economic benefits.

Public Health and Climate Benefits and Trade-Offs of U.S. Vehicle Electrification.

Vehicle electrification is a common climate change mitigation strategy, with policymakers invoking co-beneficial reductions in carbon dioxide (CO2) and air pollutant emissions. However, while previous studies of U.S. electric vehicle (EV) adoption consistently predict CO2 mitigation benefits, air quality outcomes are equivocal and depend on policies assessed and experimental parameters. We analyze climate and health co-benefits and trade-offs of six U.S. EV adoption scenarios: 25% or 75% replacement of conventional internal combustion engine vehicles, each under three different EV-charging energy generation scenarios. We transfer emissions from tailpipe to power generation plant, simulate interactions of atmospheric chemistry and meteorology using the GFDL-AM4 chemistry climate model, and assess health consequences and uncertainties using the U.S. Environmental Protection Agency Benefits Mapping Analysis Program Community Edition (BenMAP-CE). We find that 25% U.S. EV adoption, with added energy demand sourced from the present-day electric grid, annually results in a ~242 M ton reduction in CO2 emissions, 437 deaths avoided due to PM2.5 reductions (95% CI: 295, 578), and 98 deaths avoided due to lesser ozone formation (95% CI: 33, 162). Despite some regions experiencing adverse health outcomes, ~$16.8B in damages avoided are predicted. Peak CO2 reductions and health benefits occur with 75% EV adoption and increased emission-free energy sources (~$70B in damages avoided). When charging-electricity from aggressive EV adoption is combustion-only, adverse health outcomes increase substantially, highlighting the importance of low-to-zero emission power generation for greater realization of health co-benefits. Our results provide a more nuanced understanding of the transportation sector's climate change mitigation-health impact relationship.

Towards a fuller assessment of benefits to children's health of reducing air pollution and mitigating climate change due to fossil fuel combustion.

BACKGROUND: Fossil fuel combustion by-products, including particulate matter (PM2.5), polycyclic aromatic hydrocarbons (PAH), nitrogen dioxide (NO2) and carbon dioxide (CO2), are a significant threat to children's health and equality. Various policies to reduce emissions have been implemented to reduce air pollution and mitigate climate change, with sizeable estimated health and economic benefits. However, only a few adverse outcomes in children have been considered, resulting in an undercounting of the benefits to this vulnerable population. OBJECTIVES: Our goal was to expand the suite of child health outcomes addressed by programs to assess health and economic benefits, such as the Environmental Protection Agency (EPA) Benefits Mapping and Analysis Program (BenMAP), by identifying concentration-response (C-R) functions for six outcomes related to PM2.5, NO2, PAH, and/or PM10: preterm birth (PTB), low birthweight (LBW), autism, attention deficit hyperactivity disorder, IQ reduction, and the development of childhood asthma. METHODS: We conducted a systematic review of the literature published between January 1, 2000 and April 30, 2018 to identify relevant peer-reviewed case-control and cohort studies and meta-analyses. In some cases meta-analyses were available that provided reliable C-R functions and we assessed their consistency with subsequent studies. Otherwise, we reviewed all eligible studies published between our search dates. RESULTS: For each pollutant and health outcome, we present the characteristics of each selected study. We distinguish between C-R functions for endpoints having a causal or likely relationship (PTB, LBW, autism, asthma development) with the pollutants for incorporation into primary analyses and endpoints having a suggestive causal relationship with the pollutants (IQ reduction, ADHD) for secondary analyses. CONCLUSION: We have identified C-R functions for a number of adverse health outcomes in children associated with air pollutants largely from fossil fuel combustion. Their incorporation into expanded assessments of health benefits of clean air and climate mitigation policies will provide an important incentive for preventive action.

Emergency Department Visits and Ambient Temperature: Evaluating the Connection and Projecting Future Outcomes.

The U.S. Global Climate Change Research Program has identified climate change as a growing public health threat. We investigated the potential effects of changes in ambient daily maximum temperature on hyperthermia and cardiovascular emergency department (ED) visits using records for patients age 64 and younger from a private insurance database for the May-September period for 2005-2012. We found a strong positive relationship between daily maximum temperatures and ED visits for hyperthermia but not for cardiovascular conditions. Using the fitted relationship from 136 metropolitan areas, we calculated the number and rate of hyperthermia ED visits for climates representative of year 1995 (baseline period), as well as years 2050 and 2090 (future periods), for two climate change scenarios based on outcomes from five global climate models. Without considering potential adaptation or population growth and movement, we calculate that climate change alone will result in an additional 21,000-28,000 hyperthermia ED visits for May to September, with associated treatment costs between $6 million and $52 million (2015 U.S. dollars) by 2050; this increases to approximately 28,000-65,000 additional hyperthermia ED visits with treatment costs between $9 million and $118 million (2015 U.S. dollars) by 2090. The range in projected additional hyperthermia visits reflects the difference between alternative climate scenarios, and the additional range in valuation reflects different assumptions about per-case valuation.

Development of a heat vulnerability index for New York State.

OBJECTIVES: The frequency and intensity of extreme heat events are increasing in New York State (NYS) and have been linked with increased heat-related morbidity and mortality. But these effects are not uniform across the state and can vary across large regions due to regional sociodemographic and environmental factors which impact an individual's response or adaptive capacity to heat and in turn contribute to vulnerability among certain populations. We developed a heat vulnerability index (HVI) to identify heat-vulnerable populations and regions in NYS. STUDY DESIGN: Census tract level environmental and sociodemographic heat-vulnerability variables were used to develop the HVI to identify heat-vulnerable populations and areas. METHODS: Variables were identified from a comprehensive literature review and climate-health research in NYS. We obtained data from 2010 US Census Bureau and 2011 National Land Cover Database. We used principal component analysis to reduce correlated variables to fewer uncorrelated components, and then calculated the cumulative HVI for each census tract by summing up the scores across the components. The HVI was then mapped across NYS (excluding New York City) to display spatial vulnerability. The prevalence rates of heat stress were compared across HVI score categories. RESULTS: Thirteen variables were reduced to four meaningful components representing 1) social/language vulnerability; 2) socioeconomic vulnerability; 3) environmental/urban vulnerability; and 4) elderly/ social isolation. Vulnerability to heat varied spatially in NYS with the HVI showing that metropolitan areas were most vulnerable, with language barriers and socioeconomic disadvantage contributing to the most vulnerability. Reliability of the HVI was supported by preliminary results where higher rates of heat stress were collocated in the regions with the highest HVI. CONCLUSIONS: The NYS HVI showed spatial variability in heat vulnerability across the state. Mapping the HVI allows quick identification of regions in NYS that could benefit from targeted interventions. The HVI will be used as a planning tool to help allocate appropriate adaptation measures like cooling centers and issue heat alerts to mitigate effects of heat in vulnerable areas.

Predictors of summertime heat index levels in New York City apartments.

During heat waves, fatal overexposure to heat most often occurs at home. It is not known how factors such as building size, floor level, and different types of air conditioning (AC) contribute to excess indoor heat. We monitored indoor temperature and humidity in 36 apartments in New York City during summers 2014 and 2015 and used these values to calculate the indoor heat index (HI). We investigated the role of AC type and building-level factors on indoor HI using multilevel regression models. Thirty-four of 36 homes had AC. Central and ductless AC types were associated with the coolest indoor conditions; homes with window and portable AC were significantly warmer. Apartments on the top floor of a building were significantly hotter during heat advisory periods than other apartments regardless of the presence of AC. High indoor HI levels persisted in some homes for approximately 1 day following the end of the two heat advisory periods. We provide concrete evidence of higher heat levels in top floor apartments and in homes with certain types of AC. High heat levels that persist indoors after outdoor heat has subsided may present an underappreciated public health risk.

Quantitative measurement of airborne cockroach allergen in New York City apartments.

UNLABELLED: We designed and tested a sampling and analysis system for quantitative measurement of airborne cockroach allergen with sufficient sensitivity for residential exposure assessment. Integrated 1-week airborne particle samples were collected at 10-15 LPM in 19 New York City apartments in which an asthmatic child who was allergic to cockroach allergen resided. Four simultaneous air samples were collected in each home: at heights of 0.3 and 1 m in the child's bedroom and in the kitchen. Extracts of air samples were analyzed by ELISA for the cockroach allergen Bla g2, modified by amplifying the colorimetric signal generated via use of AMPLI-Q detection system (DAKO Corporation, Carpinteria, CA, USA). Settled dust samples were quantified by conventional ELISA. Of the homes where cockroach allergen was detected in settled dust, Bla g2 also was detected in 87% and 93% of air samples in the bedroom and kitchen, respectively. Airborne Bla g2 levels were highly correlated within and between the bedroom and kitchen locations (P < 0.001). Expressed as picogram per cubic meter, the room average geometric mean for Bla g2 concentrations was 1.9 pg/m³ (95% CI 0.63, 4.57) and 3.8 pg/m³ (95% CI 1.35, 9.25) in bedrooms and kitchens, respectively. This method offers an attractive supplement to settled dust sampling for cockroach allergen exposure health studies. PRACTICAL IMPLICATIONS: Until now, cockroach allergen exposures have usually been assessed by collection and analysis of settled dust, on the assumption that airborne cockroach allergen cannot be reliably measured. In this study, a sensitive and quantitative method for measuring indoor airborne exposures to cockroach allergens involving a 7-day integrated total suspended particulate (TSP) sample collected at approximately 10-15 l/min was developed. Investigators are now empowered with an alternative exposure assessment method to supplement their studies and the understanding of allergen aerodynamics in the homes of children with asthma. We report airborne cockroach allergen in apartments, suggesting an ongoing burden of inhalation exposure.

A summary of recent findings on birth outcomes and developmental effects of prenatal ETS, PAH, and pesticide exposures.

Inner-city minority populations are high-risk groups for adverse birth outcomes and also more likely to be exposed to environmental contaminants, including environmental tobacco smoke (ETS), benzo[a]pyrene B[a]P, other ambient polycyclic aromatic hydrocarbons (global PAHs), and residential pesticides. The Columbia Center for Children's Environmental Health (CCCEH) is conducting a prospective cohort study of 700 northern Manhattan pregnant women and newborns to examine the effects of prenatal exposure to these common toxicants on fetal growth, early neurodevelopment, and respiratory health. This paper summarizes results of three published studies demonstrating the effects of prenatal ETS, PAH, and pesticides on birth outcomes and/or neurocognitive development [Perera FP, Rauh V, Whyatt RM, Tsai WY, Bernert JT, Tu YH, et al. Molecular evidence of an interaction between prenatal environment exposures on birth outcomes in a multiethnic population. Environ Health Perspect 2004;12:630-62; Rauh VA, Whyatt RM, Garfinkel R, Andrews H, Hoepner L, Reyes A, et al. Developmental effects of exposure to environmental tobacco smoke and material hardship among inner-city children. Neurotoxicol Teratol 2004;26:373-85; Whyatt RM, Rauh V, Barr DB, Camann DE, Andrews HF, Garfinkel R, et al. Prenatal insecticide exposures, birth weight and length among an urban minority cohort. Environ Health Perspect, in press]. To evaluate the effects of prenatal exposure to ETS, PAHs, and pesticides, researchers analyzed questionnaire data, cord blood plasma (including biomarkers of ETS and pesticide exposure), and B[a]P-DNA adducts (a molecular dosimeter of PAHs). Self-reported ETS was associated with decreased head circumference (P = 0.04), and there was a significant interaction between ETS and adducts such that combined exposure had a significant multiplicative effect on birth weight (P = 0.04) and head circumference (P = 0.01) after adjusting for confounders. A second analysis examined the neurotoxic effects of prenatal ETS exposure and postpartum material hardship (unmet basic needs in the areas of food, housing, and clothing) on 2-year cognitive development. Both exposures depressed cognitive development (P < 0.05), and there was a significant interaction such that children with exposure to both ETS and material hardship exhibited the greatest cognitive deficit (7.1 points). A third analysis found that cord chlorpyrifos, and a combined measure of cord chlorpyrifos, diazinon, and propoxur-metabolite, were inversely associated with birth weight and/or length (P < 0.05). These results underscore the importance of policies that reduce exposure to ETS, air pollution, and pesticides with potentially adverse effects on fetal growth and child neurodevelopment.

Biomarkers in assessing residential insecticide exposures during pregnancy and effects on fetal growth.

The Columbia Center for Children's Environmental Health is using a combination of environmental and biologic measures to evaluate the effects of prenatal insecticide exposures among urban minorities in New York City. Of the 571 women enrolled, 85% report using some form of pest control during pregnancy and 46% report using exterminators, can sprays, and/or pest bombs. Chlorpyrifos, diazinon, and propoxur were detected in 99.7-100% of 48-h personal air samples collected from the mothers during pregnancy (n = 394) and in 39-70% of blood samples collected from the mothers (n = 326) and/or newborns (n = 341) at delivery. Maternal and newborn blood levels are similar and highly correlated (r = 0.4-08, P < 0.001). Levels of insecticides in blood samples and/or personal air samples decreased significantly following the 2000-2001 U.S. Environmental Protection Agency's regulatory actions to phase out residential use of chlorpyrifos and diazinon. Among infants born prior to 1/1/01, birth weight decreased by 67.3 g (95% confidence interval (CI) -116.6 to -17.8, P = 0.008) and birth length decreased by 0.43 centimeters (95% CI, -0.73 to -0.14, P = 0.004) for each unit increase in log-transformed cord plasma chlorpyrifos levels. Combined measures of (ln)cord plasma chlorpyrifos and diazinon (adjusted for relative potency) were also inversely associated with birth weight and length (P 0.8). Results support recent regulatory action to phase out residential uses of these insecticides.

Prenatal exposure, maternal sensitization, and sensitization in utero to indoor allergens in an inner-city cohort.

Primary sensitization to antigens may occur prenatally. We hypothesized that high prenatal exposure to indoor antigens increases the risk for sensitization in newborns in New York City populations with increased risk for asthma. We also investigated whether maternal sensitization is required for in utero sensitization to occur. One hundred sixty-seven pregnant African American or Dominican women residing in northern Manhattan were recruited and antigen was measured from home dust. After delivery, newborn cord and maternal blood were assayed for IgE and mononuclear cell proliferation and cytokine production in response to antigen. Cockroach, mouse, but not dust mite antigens, were commonly elevated in the kitchens and pregnant mothers' beds. Increased mononuclear cell proliferation occurred in 54% of newborns in response to cockroach, 25% in response to dust mite Dermatophagoides pteronyssinus, 40% in response to dust mite D. farinae, and 34% in response to mouse protein extracts. Antigen-induced mononuclear cell proliferation occurred in cord blood even in the absence of antigen-induced mononuclear cell proliferation in the mother. Proliferation in response to antigens did not correlate with IgE levels, but proliferation in response to dust mite extracts correlated with interluekin-5 (IL-5) production in cord blood. These results suggest that (1) high prenatal exposures to cockroach and mouse antigens are prevalent; (2) in utero sensitization to multiple indoor antigens is common, occurs to a different degree than maternal sensitization, and may involve IL-5 upregulation.

Tracking sources of bacterial contamination in stormwater discharges to Mission Bay, California.

Sources of the indicator bacteria total coliform, fecal coliform, and enterococcus were investigated in stormwater flows discharging to Mission Bay, a heavily used aquatic park in San Diego, California. Stormwater flows were targeted because long-term receiving water monitoring of the bay indicated that wet weather discharges were the predominant source of bacterial contamination. Exceedences in water quality objectives for body contact recreation established by the State of California most often occurred in the east bay, where the least amount of circulation and largest quantities of stormwater discharges occur. Unlike the wet weather results, almost all of the 89 storm drains that discharge to the bay either did not have flowing fresh water or did not contain exceedingly high bacteria densities during dry weather. Upstream tracking during multiple storm events on two of the largest watersheds draining to the bay showed that sources of indicator bacteria were diffuse and widespread. Densities were as high at the head of each watershed as they were at the mouth, where both discharged to the bay. Every reach in each creek exceeded State of California water quality objectives and had densities similar to surface flows measured before they entered the separate municipal storm sewer system from urban land uses, such as residential, commercial, and industrial, as well as open lands.

Characterization of clinical tolerance to inhaled zinc oxide in naive subjects and sheet metal workers.

Clinical tolerance to the acute effects of zinc oxide inhalation develops in workers during periods of repeated exposure. The aims of this study were to determine whether clinical tolerance is accompanied by a reduction in the acute pulmonary inflammatory and cytokine responses to zinc oxide exposure and whether tolerance can be demonstrated in sheet metal workers who chronically inhale low levels of zinc oxide. Naive (never-exposed) subjects inhaled 5 mg/m3 zinc oxide on 1 or 3 days and underwent bronchoalveolar lavage 20 hours after the final exposure. Sheet metal workers inhaled zinc oxide on 1 day and control furnace gas on another day. Among naive subjects in whom tolerance was induced, bronchoalveolar lavage fluid percent neutrophils and interleukin-6 (IL-6) levels were significantly decreased compared with subjects who underwent only a single exposure. Sheet metal workers were much less symptomatic, but they still experienced a significant increase in plasma IL-6. The results indicate that clinical tolerance to zinc oxide is accompanied by reduced pulmonary inflammation and that chronically exposed sheet metal workers are not clinically affected by exposure to zinc oxide fume at the Occupational Safety and Health Administration Permissible Exposure Limit. The increase in IL-6 levels observed in the clinically responsive, and to a lesser extent, tolerant, states following zinc oxide inhalation is consistent with the dual role of IL-6 as a pyrogen and anti-inflammatory agent.

Respiratory effects of seasonal exposures to ozone and particles.

Whereas human respiratory effects of brief ozone exposures are well documented, much less is known about the human health effects of mid- to long-term exposures. The authors' objective in this study was to determine whether lung function or respiratory symptom changes would occur over the course of a summer season among healthy young adults working outdoors in the presence of ozone. The authors studied 72 sophomore cadets from the U.S. Military Academy at West Point, New York, 21 of whom attended special summer training in Fort Dix, New Jersey, an area characterized by elevated ozone levels; the remaining cadets attended training in areas with moderate ozone levels (i.e., Fort Benning, Georgia; Fort Leonard Wood, Missouri; and Fort Sill, Oklahoma). The authors hypothesized that adverse respiratory outcomes, if any, would be more pronounced in the group exposed to higher ozone levels. Spirometry was performed and respiratory symptoms were assessed-both before and after the summer-in a clinic at West Point. Time spent outdoors during summer training averaged 11 hr/d. Both mean and peak ozone levels were higher at Fort Dix than at the three remaining sites. Regional levels of sulfur dioxide and particulate matter less than 10 microm in aerodynamic diameter were relatively low during the study. However, all cadets reported frequent exposure to dust, exhaust, and smoke in the course of their training. Averaged across all subjects, there was a statistically significant drop in forced expiratory volume in 1 sec of 44 ml (p = .035) over the summer. There were also significant increases in reports of cough, chest tightness, and sore throat at the follow-up clinic visit. A larger mean forced expiratory volume in 1 sec decline was observed at Fort Dix, where ozone exposures were the highest. The results of this study demonstrated a seasonal decline in respiratory function among healthy young adults working outdoors in the presence of ozone and particulate matter.

Air pollution and daily hospital admissions in metropolitan Los Angeles.

We used daily time-series analysis to evaluate associations between ambient carbon monoxide, nitrogen dioxide, particulate matter [less than and equal to] 10 microm in aerodynamic diameter (PM(10)), or ozone concentrations, and hospital admissions for cardiopulmonary illnesses in metropolitan Los Angeles during 1992-1995. We performed Poisson regressions for the entire patient population and for subgroups defined by season, region, or personal characteristics, allowing for effects of temporal variation, weather, and autocorrelation. CO showed the most consistently significant (p<0.05) relationships to cardiovascular admissions. A wintertime 25th-75th percentile increase in CO (1.1-2.2 ppm) predicted an increase of 4% in cardiovascular admissions. NO(2), and, to a lesser extent, PM(10) tracked CO and showed similar associations with cardiovascular disease, but O(3) was negatively or nonsignificantly associated. No significant demographic differences were found, although increased cardiovascular effects were suggested in diabetics, in whites and blacks (relative to Hispanics and Asians), and in persons older than 65 years of age. Pulmonary disease admissions associated more with NO(2) and PM(10) than with CO. Pulmonary effects were generally smaller than cardiovascular effects and were more sensitive to the choice of model. We conclude that in Los Angeles, atmospheric stagnation with high primary (CO/NO(2)/PM(10)) pollution, most common in autumn/winter, increases the risk of hospitalization for cardiopulmonary illness. Summer photochemical pollution (high O(3)) apparently presents less risk.

Airborne concentrations of PM(2.5) and diesel exhaust particles on Harlem sidewalks: a community-based pilot study.

Residents of the dense urban core neighborhoods of New York City (NYC) have expressed increasing concern about the potential human health impacts of diesel vehicle emissions. We measured concentrations of particulate matter [less than/equal to] 2.5 micro in aerodynamic diameter (PM(2.5)) and diesel exhaust particles (DEP) on sidewalks in Harlem, NYC, and tested whether spatial variations in concentrations were related to local diesel traffic density. Eight-hour (1000-1800 hr) air samples for PM(2.5 )and elemental carbon (EC) were collected for 5 days in July 1996 on sidewalks adjacent to four geographically distinct Harlem intersections. Samples were taken using portable monitors worn by study staff. Simultaneous traffic counts for diesel trucks, buses, cars, and pedestrians were carried out at each intersection on [Greater/equal to] 2 of the 5 sampling days. Eight-hour diesel vehicle counts ranged from 61 to 2,467 across the four sites. Mean concentrations of PM(2.5) exhibited only modest site-to-site variation (37-47 microg/m(3)), reflecting the importance of broader regional sources of PM(2.5). In contrast, EC concentrations varied 4-fold across sites (from 1.5 to 6 microg/m(3)), and were associated with bus and truck counts on adjacent streets and, at one site, with the presence of a bus depot. A high correlation (r = 0.95) was observed between EC concentrations measured analytically and a blackness measurement based on PM(2.5) filter reflectance, suggesting the utility of the latter as a surrogate measure of DEP in future community-based studies. These results show that local diesel sources in Harlem create spatial variations in sidewalk concentrations of DEP. The study also demonstrates the feasibility of a new paradigm for community-based research involving full and active partnership between academic scientists and community-based organizations.

Long-term residence in areas of high ozone: associations with respiratory health in a nationwide sample of nonsmoking young adults [dsee comments].

Few studies have examined the respiratory effects of multiyear ozone exposures in human populations. We examined associations between current respiratory health status and long-term ozone exposure histories in 520 Yale College (New Haven, CT) students who never smoked. Questionnaires addressed current respiratory symptoms, respiratory disease history, residential history, and other factors. The symptoms of cough, phlegm, wheeze apart from colds, and a composite respiratory symptom index (RSI) were selected as outcome measures. Forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV(1)), forced expiratory flow rate between 25 and 75% of FVC (FEF(25-75)), and forced expiratory flow rate at 75% of FVC (FEF(75)) were obtained by forced expiration into spirometers. Ozone exposure was treated as a dichotomous variable, where subjects were assigned to the high-exposure group if they lived for 4 or more years in a U.S. county with 10-year average summer-season daily 1-hr maximum ozone levels [greater/equal to] 80 ppb. Lung function and respiratory symptoms were analyzed by multiple linear and logistic regression on ozone exposure, controlling for covariates. Lung function was lower in the group with high ozone exposures: differences were statistically significant for FEV(1) [-3.1%; 95% confidence interval (CI), -0.2 to -5.9%] and FEF(25-75) (-8.1%; CI, -2.3 to -13.9%), and nearly so for FEF(75) (-6.7%; CI, 1.4 to -14.8). Gender-specific analyses revealed stronger associations for males than for females. The symptoms of chronic phlegm, wheeze apart from colds, and RSI were increased in the ozone-exposed group, with odds ratios of 1.79 (CI, 0.83-3.82), 1.97 (CI, 1.06-3.66), and 2.00 (CI, 1.15-3.46), respectively. We conclude that living for 4 or more years in regions of the country with high levels of ozone and related copollutants is associated with diminished lung function and more frequent reports of respiratory symptoms.

Diesel exhaust exposure among adolescents in Harlem: a community-driven study.

OBJECTIVES: This study sought individual-level data on diesel exhaust exposure and lung function among adolescents in Harlem as part of a community-driven research agenda. METHODS: High school students administered in-person surveys to seventh grade students to ascertain information on demographics, asthma history, and self-reported and maternal smoking. Urine samples were assayed for 1-hydroxypyrene (1-HP), a marker of diesel exhaust exposure, and cotinine, a marker of tobacco smoke exposure. Computer-assisted spirometry was used to measure lung function. RESULTS: Three quarters (76%) of the participating students had detectable levels of 1-HP. Three students (13%) had an FEF25-75 of less than or equal to 80% of their predicted measurements, and 4 students (17%) had results between 80% and 90% of the predicted value, all of which are suggestive of possible lung impairment. CONCLUSIONS: These data suggest that most adolescents in Harlem are exposed to detectable levels of diesel exhaust, a known exacerbator and possible cause of chronic lung disorders such as asthma. Community-driven research initiatives are important for empowering communities to make needed changes to improve their environments and health.

Methods development for epidemiologic investigations of the health effects of prolonged ozone exposure. Part III. An approach to retrospective estimation of lifetime ozone exposure using a questionnaire and ambient monitoring data (U.S. sites).

Methods are needed for retrospective estimation of long-term ozone exposures in epidemiologic studies. The overall objective of this study was to evaluate whether data from available U.S. ozone monitoring sites are useful for estimating lifetime ozone exposures of young adults (for example, college students). Several aspects of this question were evaluated. First, we applied and (compared several spatial interpolation methods to a set of long-term average ozone data from all U.S. monitoring sites in operation from 1981 through 1990. Interpolation methods included simple and weighted averages, linear regression, and, in an exploratory way, kriging. The comparison of methods was carried out for five different metrics of ozone concentration: the daily one-hour maximum (MAX1) and eight-hour maximum (MAX8), the average ozone concentrations between 10 a.m. and 6 p.m. (MID8) and between 10 a.m. and 10 p.m. (MID12), and the sum of all hourly ozone concentrations greater than or equal to 60 parts per billion (ppb) (SUM06). We also tested whether interpolations were improved by modeling the influence of covariates such as population density, elevation, and weather on ozone concentrations. We analyzed the reliability of a set of newly developed questions about past activity levels among a group of 52 freshmen students at Yale University. This was done by analyzing the agreement between answers to the same questionnaire administered two times, one month apart (test and retest), to the same students. Finally, we combined the interpolation models with residential history information obtained by questionnaire to derive long-term ozone exposure estimates for a group of 200 Yale freshmen. Results of our study showed that the density of available monitoring sites appears to be adequate for estimating spatial patterns of long-term average ambient ozone concentrations. A simple regression-based interpolation on the three nearest sites produced consistently good results. Including covariates in the interpolation models did not substantially improve the estimates. The largest estimation errors occurred for areas where ozone concentrations were highest. The newly developed activity history questions exhibited fair to moderate reliability, The results of this work imply that reasonably precise estimates of long-term ambient ozone concentrations for use in large-scale epidemiologic studies can be achieved by interpolating ozone concentrations between available U.S. monitoring sites. This study did not address the issues of whether and how retrospective data on factors that modify exposure or dose (e.g., indoor/outdoor penetration of ozone and time outdoors) can be used to derive estimates of long-term personal ozone exposures and contribute to the assessment of received dose.

Thoughts of agoraphobic people during scary tasks.

The authors examined the occurrence of theoretically derived patterns of thinking in 74 agoraphobic participants as they drove alone or tolerated an enclosed place. During the increasingly scary tasks in a behavioral test hierarchy, participants responded to a periodic beep by stating aloud what they were thinking at that moment, yielding more than 1,800 tape-recorded statements. Content analyses revealed that participants were mainly preoccupied with their current anxiety (expressed in 29% of the statements) and with their self-efficacy (15%). Despite participants' mounting feelings of anxiety, fewer than 1% of their statements expressed a thought of danger or an anticipation of future anxiety or panic. The rarity of danger thoughts poses an explanatory challenge for all cognitive theories of phobia and especially for the perceived danger theory of A. T. Beck (1976) and A. T. Beck, G. Emery, and R. L. Greenberg (1985).

Metal fume fever: characterization of clinical and plasma IL-6 responses in controlled human exposures to zinc oxide fume at and below the threshold limit value.

Results from animal and preliminary human exposure studies have called into question whether the 5 mg/m3 8-hour time-weighted average threshold limit value (TLV) for zinc oxide fume is sufficient to protect workers against metal fume fever. The objectives of this study were to determine the clinical effects of exposures to low concentrations of zinc oxide and to ascertain whether these exposures elevated circulating levels of specific cytokines, which could account for the symptoms of the metal fume fever syndrome. Thirteen resting naive subjects inhaled, on separate days, air and 2.5 and 5 mg/m3 of furnace-generated zinc oxide fume for 2 hours. Subjects recorded symptoms and temperature and had blood drawn before and after each exposure. The mean (+/- SE) maximum rise in oral temperature at 6 to 12 hours after exposure was 1.4 +/- 0.3 degrees F after 5 mg/m3, compared with 0.6 +/- 0.5 degrees F after air exposure (P < 0.05). Mean temperature was also elevated after exposure to 2.5 mg/m3 zinc oxide (1.2 +/- 0.3 degrees F). In a parallel fashion, plasma levels of interleukin 6 (IL-6), a pyrogen, were significantly elevated after exposure to 5 mg/m3 zinc oxide. Mean IL-6 values (pg/mL) at pre-exposure and at 3 and 6 hours post-exposure were 1.9 (+/- 0.6), 2.8 (+/- 0.7), and 2.9 (+/- 0.6), respectively, on the air day and 1.6 (+/- 0.6), 4.4 (+/- 1.2), and 6.4 (+/- 1.1) on the 5 mg/m3 zinc oxide day. Zinc oxide exposure did not significantly affect plasma levels of tumor necrosis factor. Total symptom scores peaked 9 hours after the 5 mg/m3 zinc oxide exposure. Myalgias, cough, and fatigue were the predominant symptoms reported. Inhalation of zinc oxide for 2 hours at the current TLV of 5 mg/m3 produces fever and symptoms along with elevation in plasma IL-6 levels.