Association between coarse particulate matter and inflammatory and hemostatic markers in a cohort of midlife women.

BACKGROUND: Exposure to particulate matter air pollution has been associated with cardiovascular disease (CVD) morbidity and mortality; however, most studies have focused on fine particulate matter (PM2.5) exposure and CVD. Coarse particulate matter (PM10-2.5) exposure has not been extensively studied, particularly for long-term exposure, and the biological mechanisms remain uncertain. METHODS: We examined the association between ambient concentrations of PM10-2.5 and inflammatory and hemostatic makers that have been linked to CVD. Annual questionnaire and clinical data were obtained from 1694 women (≥ 55 years old in 1999) enrolled in the longitudinal Study of Women's Health Across the Nation (SWAN) at six study sites from 1999 to 2004. Residential locations and the USEPA air monitoring network measurements were used to assign exposure to one-year PM10-2.5, as well as co-pollutants. Linear mixed-effects regression models were used to describe the association between PM10-2.5 exposure and markers, including demographic, health and other covariates. RESULTS: Each interquartile (4 µg/m3) increase in one-year PM10-2.5 exposure was associated with a 5.5% (95% confidence interval [CI]: 1.8, 9.4%) increase in levels of plasminogen activator inhibitor-1 (PAI-1) and 4.1% (95% CI: - 0.1, 8.6%) increase in high-sensitivity C-creative Protein (hs-CRP). Stratified analyses suggested that the association with PAI-1 was particularly strong in some subgroups, including women who were peri-menopausal, were less educated, had a body mass index lower than 25, and reported low alcohol consumption. The association between PM10-2.5 and PAI-1 remained unchanged with adjustment for PM2.5, ozone, nitrogen dioxide, and carbon monoxide. CONCLUSIONS: Long-term PM10-2.5 exposure may be associated with changes in coagulation independently from PM2.5, and thus, contribute to CVD risk in midlife women.

Associations between fine particulate matter and changes in lipids/lipoproteins among midlife women.

Fine particles (PM2.5) are known to increase risks of cardiovascular diseases, but it is unclear how they affect plasma lipid levels. In this study, we examined the associations between PM2.5 exposure and lipid/lipoprotein levels from 2289 midlife women enrolled in the longitudinal Study of Women's Health Across the Nation. The average exposure to PM2.5 and gaseous co-pollutants during the prior one year, six months, 30 days, and one day were estimated for each woman based on U.S. Environmental Protection Agency ambient monitoring data. Blood samples were collected annually from 1999 to 2005 and analyzed for lipids/lipoproteins. Mixed-effect models were used to account for repeated measures for each woman, adjusted for demographic, health and behavior covariates. PM2.5 exposures, especially the long-term exposure, were negatively associated with protective lipoproteins, and positively associated with atherogenic lipoproteins. For example, each 3 µg/m3 increase of one-year PM2.5 exposure was associated with decreases of -0.7% (-1.4%, -0.1%) in high-density lipoprotein cholesterols and -0.6% (-1.1%, -0.1%) in apolipoprotein A1 (ApoA1), as well as increases of 3.8% (1.0%, 6.6%) in lipoprotein(a) and 1.4% (0.5%, 2.3%) in the ratio of apolipoprotein B (ApoB)/ApoA1. In stratified analysis, increased atherogenic lipoproteins were mainly observed in women without dyslipidemia, and both increased atherogenic lipoproteins and reduced protective lipoproteins were observed among women in perimenopause. In summary, PM2.5 exposure was associated with adverse lipid level changes, and thus, may increase cardiovascular risks in midlife women.

Residential Exposure to PM2.5 and Ozone and Progression of Subclinical Atherosclerosis Among Women Transitioning Through Menopause: The Study of Women's Health Across the Nation.

Objective: This article aims to examine the association between long-term ambient air pollution and progression of subclinical atherosclerosis with 2-year follow-up among midlife women from the Study of Women's Health Across the Nation (SWAN). Materials and Methods: Carotid duplex ultrasonography was performed in participants from a SWAN ancillary study carried out at the Pittsburgh and Chicago sites. Mean and maximum carotid intima-media thickness (CIMT) and plaque burden were assessed throughout the common, bulb, and internal carotid artery. The yearly mean exposure to PM2.5 (particulate matter) and ozone was generated based on monitors within 20 km of the participants' home. The effect of air pollutants during follow-up on progression of CIMT was estimated using linear mixed-effects models, and the effect on progression of plaque presence and plaque index, a measure of extent of plaque, was evaluated using logistic regression. Results: This study included 417 (257 White and 160 Black) women with a mean age of 51 years at baseline. A 1 µg/m3 higher yearly mean exposure to PM2.5 during follow-up was associated with a 4.28 (95% confidence interval [CI]: 0.02-8.54) µm/year increase in maximum CIMT, after adjusting for socioeconomic and traditional cardiovascular disease (CVD) risk factors. Exposure to PM2.5 contributed to a 30% (95% CI: 3%-65%) higher odds of plaque index progression adjusting for socioeconomic factors only. Conclusions: PM2.5 independently contributed to progression of subclinical atherosclerosis, among women transitioning through menopause, a time of increasing CVD risk. Yet no significant associations between ozone and subclinical atherosclerosis were observed.

Five-year exposure to PM2.5 and ozone and subclinical atherosclerosis in late midlife women: The Study of Women's Health Across the Nation.

INTRODUCTION: Effects of more than one-year exposure to air pollution on atherosclerosis is seldom studied. This paper aims to examine the association between five-year exposure to particulate matter ≤2.5 µm (PM2.5), ozone (O3) and atherosclerosis observed about seven years later in late midlife women. MATERIAL AND METHODS: This study was conducted among 1188 women of the Study of Women's Health Across the Nation (SWAN) from five sites, Detroit, MI; Oakland, CA; Pittsburgh, PA; Chicago, IL; and Newark, NJ, with available data on both air pollutant exposure and carotid ultrasound scans. Five-year mean annualized exposure levels of two air pollutants, PM2.5 and ozone (O3), were collected during 5 SWAN visits (1999-2005) from monitors 20 km within the participant's residential address. Linear regression models were used to estimate the association of prior five-year mean annualized exposure to PM2.5 and O3 with common carotid intima-media thickness (cIMT) and inter-adventitial diameter (IAD) examined approximately seven years later (2009-2013). Logistic and multinomial logistic regressions were applied to assess the associations of air pollutants with plaque presence and plaque index, respectively. RESULTS: At time of carotid ultrasound scan, women were on average 59.6 (±2.7) years old and a majority was postmenopausal (88.4%). The women were White (48.4%), Black (31.2%), Chinese (13.3%) and Hispanic (7.1%). A 1 µg/m3 higher 5-year mean annualized exposure to PM2.5 was associated with an 8.0 µm (95% CI: 1.0-15.1) greater maximum cIMT at a later mid-life, adjusting for cardiovascular disease risk factors; but was only related to IAD after adjusting for site. No association was found between either pollutant and plaque presence or plaque index. CONCLUSIONS: Long-term exposure to PM2.5 may contribute to elevated risk of atherosclerosis in the post-menopausal period.

Association between gaseous air pollutants and inflammatory, hemostatic and lipid markers in a cohort of midlife women.

BACKGROUND: Exposures to ambient gaseous pollutants have been linked to cardiovascular diseases (CVDs), but the biological mechanisms remain uncertain. OBJECTIVES: This study examined the changes in CVD marker levels resulting from elevated exposure to ambient gaseous pollutants in midlife women. METHODS: Annual repeated measurements of several inflammatory, hemostatic and lipid makers were obtained from 2306 midlife women enrolled in the longitudinal Study of Women's Health Across the Nation (SWAN) between 1999 and 2004. Ambient carbon monoxide (CO), nitrogen dioxide (NO2), and sulfur dioxide (SO2) data were assigned to each woman based on proximity of the monitoring station to her residential address. Short- and long-term exposures were calculated, and their associations with markers were examined using linear mixed-effects regression models, adjusted for demographic, health and other factors. RESULTS: Short-term CO exposure was associated with increased fibrinogen, i.e., every interquartile increase of average prior one-week exposure to CO was associated with 1.3% (95% CI: 0.6%, 2.0%) increase in fibrinogen. Long-term exposures to NO2 and SO2 were associated with reduced high-density lipoproteins and apolipoprotein A1, e.g., 4.0% (1.7%, 6.3%) and 4.7% (2.8%, 6.6%) decrease per interquartile increment in prior one-year average NO2 concentration, respectively. Fine particle (PM2.5) exposure confounded associations between CO/NO2 and inflammatory/hemostatic markers, while associations with lipoproteins were generally robust to PM2.5 adjustment. CONCLUSIONS: Exposures to these gas pollutants at current ambient levels may increase thrombotic potential and disrupt cholesterol metabolism, contributing to greater risk of CVDs in midlife women. Caution should be exercised in evaluating the confounding by PM2.5 exposure.

Estimating the associations of apparent temperature and inflammatory, hemostatic, and lipid markers in a cohort of midlife women.

Associations between temperature and cardiovascular (CVD) mortality have been reported, but the underlying biological mechanisms remain uncertain. We explored the association between apparent temperature and serum biomarkers for CVD. Using linear mixed effects models, we examined the relationships between residence-proximate apparent temperature (same day and 1, 7, and 30 days prior) and several inflammatory, hemostatic, and lipid biomarkers for midlife women from 1999 through 2004. Our study population consisted of 2,306 women with mean age of 51 years (± 3 years) enrolled in Study of Women's Health Across the Nation (SWAN) in Chicago, Illinois; Detroit, Michigan; Los Angeles and Oakland, California; Newark, New Jersey; and Pittsburgh, Pennsylvania. Mean daily apparent temperature was calculated using temperature and relative humidity data provided by the National Climatic Data Center and the US Environmental Protection Agency, while daily data for fine particles, ozone, carbon monoxide, and nitrogen dioxide from the US Environmental Protection Agency Air Quality Data Mart were considered as confounders. All analyses were stratified by warm and cold seasons. More significant (p < 0.10) negative associations were found during the warm season for various lag times, including hs-CRP, fibrinogen, tissue plasminogen activator antigen (tPA-ag), tissue plasminogen activator antigen (PAI-1), Factor VIIc, high-density lipoprotein (HDL), and total cholesterol. During the cold season, significant negative associations for fibrinogen and HDL, but significant positive associations for tPA-ag, PAI-1, and triglycerides were observed for various lag times. With the exception of ozone, pollutants did not confound these associations. Apparent temperature was associated with several serum biomarkers of CVD risk in midlife women, shedding light on potential mechanisms.

Long- and Short-term Exposure to Air Pollution and Inflammatory/Hemostatic Markers in Midlife Women.

BACKGROUND: Studies have reported associations between long-term air pollution exposures and cardiovascular mortality. The biological mechanisms connecting them remain uncertain. METHODS: We examined associations of fine particles (PM2.5) and ozone with serum markers of cardiovascular disease risk in a cohort of midlife women. We obtained information from women enrolled at six sites in the multi-ethnic, longitudinal Study of Women's Health Across the Nation, including repeated measurements of high-sensitivity C-reactive protein, fibrinogen, tissue-type plasminogen activator antigen, plasminogen activator inhibitor type 1, and factor VIIc (factor VII coagulant activity). We obtained residence-proximate PM2.5 and ozone monitoring data for a maximum five annual visits, calculating prior year, 6-month, 1-month, and 1-day exposures and their relations to serum markers using longitudinal mixed models. RESULTS: For the 2,086 women studied from 1999 to 2004, PM2.5 exposures were associated with all blood markers except factor VIIc after adjusting for age, race/ethnicity, education, site, body mass index, smoking, and recent alcohol use. Adjusted associations were strongest for prior year exposures for high-sensitivity C-reactive protein (21% increase per 10 µg/m³ PM2.5, 95% confidence interval [CI]: 6.6, 37), tissue-type plasminogen activator antigen (8.6%, 95% CI: 1.8, 16), and plasminogen activator inhibitor (35%, 95% CI: 19, 53). An association was also observed between year prior ozone exposure and factor VIIc (5.7% increase per 10 ppb ozone, 95% CI: 2.9, 8.5). CONCLUSIONS: Our findings suggest that prior year exposures to PM2.5 and ozone are associated with adverse effects on inflammatory and hemostatic pathways for cardiovascular outcomes in midlife women.

A Time-Stratified Case-Crossover Study of Ambient Ozone Exposure and Emergency Department Visits for Specific Respiratory Diagnoses in California (2005-2008).

BACKGROUND: Studies have explored ozone's connection to asthma and total respiratory emergency department visits (EDVs) but have neglected other specific respiratory diagnoses despite hypotheses relating ozone to respiratory infections and allergic responses. OBJECTIVE: We examined relationships between ozone and EDVs for respiratory visits, including specifically acute respiratory infections (ARI), asthma, pneumonia, chronic obstructive pulmonary disease (COPD), and upper respiratory tract inflammation (URTI). METHODS: We conducted a multi-site time-stratified case-crossover study of ozone exposures for approximately 3.7 million respiratory EDVs from 2005 through 2008 among California residents living within 20 km of an ozone monitor. Conditional logistic regression was used to estimate associations by climate zone. Random effects meta-analysis was then applied to estimate pooled excess risks (ER). Effect modification by season, distance from the monitor and individual demographic characteristics (i.e., age, race/ethnicity, sex, and payment method), and confounding by other gaseous air pollutants were also investigated. Meta-regression was utilized to explore how climate zone-level meteorological, demographic, and regional differences influenced estimates. RESULTS: We observed ozone-associated increases in all respiratory, asthma, and ARI visits, which were slightly larger in the warm season [asthma ER per 10-ppb increase in mean of same and previous 3 days ozone exposure (lag03) = 2.7%, 95% CI: 1.5, 3.9; ARI ERlag03 = 1.4%, 95% CI: 0.8, 1.9]. EDVs for pneumonia, COPD, and URTI were also significantly associated with ozone exposure over the whole year, but typically more consistently so during the warm season. CONCLUSIONS: Short-term ozone exposures among California residents living near an ozone monitor were positively associated with EDVs for asthma, ARI, pneumonia, COPD, and URTI from 2005 through 2008. Those associations were typically larger and more consistent during the warm season. Our findings suggest that these outcomes should be considered when evaluating the potential health benefits of reducing ozone concentrations. CITATION: Malig BJ, Pearson DL, Chang YB, Broadwin R, Basu R, Green RS, Ostro B. 2016. A time-stratified case-crossover study of ambient ozone exposure and emergency department visits for specific respiratory diagnoses in California (2005-2008). Environ Health Perspect 124:745-753; http://dx.doi.org/10.1289/ehp.1409495.

A Case-Crossover Study of Temperature and Infant Mortality in California.

BACKGROUND: While most research on temperature and mortality has focused on the elderly, little has concentrated on infants, who may also lack thermoregulatory responses to heat exposure. METHODS: We examined mean daily apparent temperature, a combination of temperature and humidity, and infant deaths in California during the warm season of May through October 1999 to 2011. Deaths from all causes and specifically from congenital malformations, sudden infant death syndrome, abnormal gestation duration, respiratory causes, and circulatory causes were considered in a time-stratified case-crossover analysis of 12 356 infant deaths. RESULTS: For all-cause mortality, excess risk was 4.4% (95% confidence interval -0.3, 9.2) per 5.6°C increase for average of same day and previous 3 days apparent temperature (lag 03). The associations for apparent temperature and both all-cause mortality and deaths caused by gestation duration were highest for Black infants (13.3%, 95% CI 0.6, 27.6 and 23.7%, 95% CI -3.3, 58.2, respectively), while White infants had elevated risk for deaths from respiratory causes (44.6%; -0.7, 110.5). We further observed differential effects for neonates (infants aged 28 days and under) and post-neonates (infants above 28 days and under 1 year), and coastal and non-coastal regions. These associations remained even after considering criteria air pollutants. CONCLUSIONS: This study suggests that infants are a vulnerable subgroup to heat exposure. Further studies should be conducted with a sufficient number of cases of infant deaths in other locales.

Chronic PM2.5 exposure and inflammation: determining sensitive subgroups in mid-life women.

BACKGROUND: Several cohort studies report associations between chronic exposure to ambient fine particles (PM2.5) and cardiovascular mortality. Uncertainty exists about biological mechanisms responsible for this observation, but systemic inflammation has been postulated. In addition, the subgroups susceptible to inflammation have not been fully elucidated. METHODS: We investigated whether certain subgroups are susceptible to the effects of long-term exposure to PM2.5 on C-reactive protein (CRP), a marker of inflammation directly linked to subsequent cardiovascular disease. We used data from the SWAN cohort of 1923 mid-life women with up to five annual repeated measures of CRP. Linear mixed and GEE models accounting for repeated measurements within an individual were used to estimate the effects of prior-year PM2.5 exposure on CRP. We examined CRP as a continuous and as binary outcome for CRP greater than 3mg/l, a level of clinical significance. RESULTS: We found strong associations between PM2.5 and CRP among several subgroups. For example a 10 µg/m(3) increase in annual PM2.5 more than doubled the risk of CRP greater than 3mg/l in older diabetics, smokers and the unmarried. Larger effects were also observed among those with low income, high blood pressure, or who were using hormone therapy, with indications of a protective effects for those using statins or consuming moderate amounts of alcohol. CONCLUSIONS: In this study, we observed significant associations between long-term exposure to PM2.5 and CRP in several susceptible subgroups. This suggests a plausible pathway by which exposure to particulate matter may be associated with increased risk of cardiovascular disease.

Effects of fine particulate matter and its constituents on low birth weight among full-term infants in California.

Relationships between prenatal exposure to fine particles (PM2.5) and birth weight have been observed previously. Few studies have investigated specific constituents of PM2.5, which may identify sources and major contributors of risk. We examined the effects of trimester and full gestational prenatal exposures to PM2.5 mass and 23 PM2.5 constituents on birth weight among 646,296 term births in California between 2000 and 2006. We used linear and logistic regression models to assess associations between exposures and birth weight and risk of low birth weight (LBW; <2500g), respectively. Models were adjusted for individual demographic characteristics, apparent temperature, month and year of birth, region, and socioeconomic indicators. Higher full gestational exposures to PM2.5 mass and several PM2.5 constituents were significantly associated with reductions in term birth weight. The largest reductions in birth weight were associated with exposure to vanadium, sulfur, sulfate, iron, elemental carbon, titanium, manganese, bromine, ammonium, zinc, and copper. Several of these PM2.5 constituents were associated with increased risk of term LBW. Reductions in birth weight were generally larger among younger mothers and varied by race/ethnicity. Exposure to specific constituents of PM2.5, especially traffic-related particles, sulfur constituents, and metals, were associated with decreased birth weight in California.

Coarse particles and respiratory emergency department visits in California.

Although respiratory disease has been strongly connected to fine particulate air pollution (particulate matter <2.5 µm in diameter (PM2.5)), evidence has been mixed regarding the effects of coarse particles (particulate matter from 2.5 to 10 µm in diameter), possibly because of the greater spatial heterogeneity of coarse particles. In this study, we evaluated the relationship between coarse particles and respiratory emergency department visits, including common subdiagnoses, from 2005 to 2008 in 35 California counties. A time-stratified case-crossover design was used to help control for time-invariant confounders and seasonal influences, and the study population was limited to those residing within 20 km of pollution monitors to mitigate the influence of spatial heterogeneity. Significant associations between respiratory emergency department visits and coarse particle levels were observed. Asthma visits showed associations (for 2-day lag, excess risk per 10 µg/m³ = 3.3%, 95% confidence interval: 2.0, 4.6) that were robust to adjustment by other common air pollutants (particles <2.5 µm in diameter, ozone, nitrogen dioxide, carbon monoxide, and sulfur dioxide). Pneumonia and acute respiratory infection visits were not associated, although some suggestion of a relationship with chronic obstructive pulmonary disease visits was present. Our results indicate that coarse particle exposure may trigger asthma exacerbations requiring emergency care, and reducing exposures among asthmatic persons may provide benefits.

The effect of high ambient temperature on emergency room visits.

BACKGROUND: The association between temperature and mortality has been widely researched, although the association between temperature and morbidity has been less studied. We examined the association between mean daily apparent temperature and emergency room (ER) visits in California. METHODS: We used a time-stratified case-crossover design, restricting our data to the warm seasons of 2005-2008 in 16 climate zones. The study population included cases residing within 10 km of meteorologic monitors. Conditional logistic regression models with apparent temperature were applied by climate zone; these models were then combined in meta-analyses to estimate overall effects. Our analyses considered the effects by disease subgroup, race/ethnic group, age group, and potential confounding by air pollutants. RESULTS: More than 1.2 million ER visits were included. Positive associations were found for same-day apparent temperature and ischemic heart disease (% excess risk per 10°F = 1.7 [95% confidence interval = 0.2 to 3.3]), ischemic stroke (2.8 [0.9 to 4.7]), cardiac dysrhythmia (2.8 [0.9 to 4.9]), hypotension (12.7 [8.3 to 17.4]), diabetes (4.3 [2.8 to 5.9]), intestinal infection (6.1 [3.3 to 9.0]), dehydration (25.6 [21.9 to 29.4]), acute renal failure (15.9 [12.7 to 19.3]), and heat illness (393.3 [331.2 to 464.5]). Negative associations were found for aneurysm, hemorrhagic stroke, and hypertension. Most of these estimates remained relatively unchanged after adjusting for air pollutants. Risks often varied by age or racial/ethnic group. CONCLUSIONS: Increased temperatures were found to have same-day effects on ER admission for several outcomes. Age and race/ethnicity seemed to modify some of these impacts.

The effect of temperature on hospital admissions in nine California counties.

OBJECTIVES: This study examined the association between mean daily apparent temperature and hospital admissions for several diseases in nine California counties from May to September, 1999 to 2005. METHODS: We conducted a time-stratified case-crossover study limited to cases with residential zip codes located within 10 km of a temperature monitor. County-specific estimates were combined, using a random effects meta-analysis. The analyses also considered the effects of ozone and particulate matter (PM(2.5)). RESULTS: We found that a 10 degrees F increase in mean apparent temperature was associated with a 3.5% [95% confidence interval (CI) 1.5-5.6] increase in ischemic stroke and increases in several other disease-specific outcomes including all respiratory diseases (2.0%, 95% CI 0.7-3.2), pneumonia (3.7%, 95% CI 1.7-3.7), dehydration (10.8%, 95% CI 8.3-13.6), diabetes (3.1%, 95% CI 0.4-5.9), and acute renal failure (7.4%, 95% CI 4.0-10.9). There was little evidence that the temperature effects we found were due to confounding by either PM(2.5) or ozone. CONCLUSION: Our results indicate that increases in ambient temperature have important public health impacts on morbidity.

Developing asthma in childhood from exposure to secondhand tobacco smoke: insights from a meta-regression: [review] / Asma na infância por exposição ao tabagismo passivo: compreensão a partir de uma meta-regressão: [revisão]

Studies have shown links between household secondhand tobacco smoke (SHS) exposure and induction of childhood asthma. But the true nature of this link remains unclear in many studies. We conducted a meta-analysis of studies published from 1970 to 2005 to uncover consistent patterns of relative risk estimates (RRs), and found substantial heterogeneity within initial summary RRs of 1.48 [95 percent confidence interval (CI), 1.32-1.65], 1.25 (1.21-1.30), and 1.21 (1.08-1.36), for ever, current, and incident asthma, respectively. Lack of control for type of atopy history (familial or child) and child's own smoking status within studies and age category altered summary RRs in separate metaregressions. After adjustments, consistent patterns of association emerged between SHS exposure and childhood asthma induction. Our summary RR of 1.33 (95 percent CI, 1.14-1.56) from studies of incident asthma among older children (618 years old) is 1.27 times the estimate from studies of younger children and higher than estimates from earlier meta-analyses. This showns that exposure duration may be a more important factor than previously understood, and suggests that SHS could be a more fundamental cause of childhood asthma than some previous meta-analyses have indicated.

Diversos estudos demonstraram a ligação entre a exposição ao tabagismo passivo domiciliar (TPD) e a ocorrência de asma na infância. A verdadeira natureza desta ligação, no entanto, continua não esclarecida em muitos deles. Uma meta-análise de estudos publicados entre 1970 e 2005 conduzida a fim de revelar padrões consistentes de estimativas de risco relativas (RRs) revelou heterogeneidade substancial do RR sumário inicial de 1,48 [intervalo de confidência (IC) de 95 percent , 1,32-1,65], 1,25 (1,21-1,30), e 1,21 (1,08-1,36), e de 1,21 (1,08-1,36), para a asma intermitente e persistente, respectivamente. A falta de controles para tipos de história de atopia (familiar ou da criança) e sobre a condição de fumante da própria criança, assim como de faixas etárias, alterou os RRs em meta-regressões individuais. Após ajustes, emergiram padrões de associação consistentes entre exposição ao TPD e asma infantil. Nosso RR sumário de 1,33 (95 percent CI, 1,14-1,56) dos estudos de asma intermitente entre crianças maiores (entre 6 e 18 anos) é 1,27 vezes a estimativa de estudos feitos com crianças menores, além de ser maior do que as estimativas de meta-análises anteriores. Isto demonstra que a duração da exposição pode ser um fator mais importante do que se pensava, e sugere a exposição ao TPD como causa mais fundamental de asma na infância do que indicado em estudos anteriores.

Evaluation and application of the RD50 for determining acceptable exposure levels of airborne sensory irritants for the general public.

BACKGROUND: The RD(50) (exposure concentration producing a 50% respiratory rate decrease) test evaluates airborne chemicals for sensory irritation and has become an American Society for Testing and Materials (ASTM) standard method. Past studies reported good correlations (R(2)) between RD(50)s and the occupational exposure limits, particularly threshold limit values (TLVs). OBJECTIVE: The main purpose of this study was to examine the relationship between RD(50)s and human sensory irritation responses in a quantitative manner, particularly for chemicals that produce burning sensation of the eyes, nose, or throat, based on lowest observed adverse effect levels (LOAELs) reported for human subjects. METHODS: We compared RD(50)s with LOAELs and acute reference exposure levels (RELs). RELs, developed by the California Environmental Protection Agency's Office of Environmental Health Hazard Assessment, represent a level at which no adverse effects are anticipated after exposure. We collected RD(50)s from the published literature and evaluated them for consistency with ASTM procedures. We identified LOAELs for human irritation and found 25 chemicals with a corresponding RD(50) in mice. DISCUSSION: We found the relationship between RD(50)s and LOAELs as log RD(50) = 1.16 (log LOAEL) + 0.77 with an R(2) value of 0.80. This strong correlation supports the use of the RD(50) in establishing exposure limits for the public. We further identified 16 chemical irritants with both RD(50)s and corresponding acute RELs, and calculated the relationship as log RD(50) = 0.71 (log REL) + 2.55 with an R(2) value of 0.71. This relationship could be used to identify health protective values for the public to prevent respiratory or sensory irritation. CONCLUSION: Consequently, we believe that the RD(50) has benefits for use in setting protective levels for the health of both workers and the general population.

Developing asthma in childhood from exposure to secondhand tobacco smoke: insights from a meta-regression.

OBJECTIVE: Studies have identified associations between household secondhand tobacco smoke (SHS) exposure and induction of childhood asthma. However, the true nature and strength of this association remains confounded in many studies, producing inconsistent evidence. To look for sources of potential bias and try to uncover consistent patterns of relative risk estimates (RRs), we conducted a meta-analysis of studies published between 1970 and 2005. DATA SOURCES: Through an extensive literature search, we identified 38 epidemiologic studies of SHS exposure and the development of childhood asthma (that also controlled for atopy history) from 300 potentially relevant articles. DATA SYNTHESIS: We observed substantial heterogeneity within initial summary RRs of 1.48 [95% confidence interval (CI), 1.32-1.65], 1.25 (1.21-1.30), and 1.21 (1.08-1.36), for ever, current, and incident asthma, respectively. Lack of control for type of atopy history (familial or child) and child's own smoking status within studies and age category altered summary RRs in separate meta-regressions. After adjusting for these confounding characteristics, consistent patterns of association emerged between SHS exposure and childhood asthma induction. Our summary RR of 1.33 (95% CI, 1.14-1.56) from studies of incident asthma among older children (6-18 years of age) is 1.27 times the estimate from studies of younger children and higher than estimates reported in earlier meta-analyses. CONCLUSIONS: This new finding indicates that exposure duration may be a more important factor in the induction of asthma than previously understood, and suggests that SHS could be a more fundamental and widespread cause of childhood asthma than some previous meta-analyses have indicated.

The effects of components of fine particulate air pollution on mortality in california: results from CALFINE.

OBJECTIVE: Several epidemiologic studies provide evidence of an association between daily mortality and particulate matter < 2.5 pm in diameter (PM2.5). Little is known, however, about the relative effects of PM2.5 constituents. We examined associations between 19 PM2.5 components and daily mortality in six California counties. DESIGN: We obtained daily data from 2000 to 2003 on mortality and PM2.5 mass and components, including elemental and organic carbon (EC and OC), nitrates, sulfates, and various metals. We examined associations of PM2.5 and its constituents with daily counts of several mortality categories: all-cause, cardiovascular, respiratory, and mortality age > 65 years. Poisson regressions incorporating natural splines were used to control for time-varying covariates. Effect estimates were determined for each component in each county and then combined using a random-effects model. RESULTS: PM2.5 mass and several constituents were associated with multiple mortality categories, especially cardiovascular deaths. For example, for a 3-day lag, the latter increased by 1.6, 2.1, 1.6, and 1.5% for PM2.5, EC, OC, and nitrates based on interquartile ranges of 14.6, 0.8, 4.6, and 5.5 pg/m(3), respectively. Stronger associations were observed between mortality and additional pollutants, including sulfates and several metals, during the cool season. CONCLUSION: This multicounty analysis adds to the growing body of evidence linking PM2.5 with mortality and indicates that excess risks may vary among specific PM2.5 components. Therefore, the use of regression coefficients based on PM2.5 mass may underestimate associations with some PM2.5 components. Also, our findings support the hypothesis that combustion-associated pollutants are particularly important in California.

The association between exposure to environmental tobacco smoke and breast cancer: a review by the California Environmental Protection Agency.

BACKGROUND: The California Environmental Protection Agency (Cal/EPA) recently completed a health effects assessment of exposure to environmental tobacco smoke (ETS) which resulted in California listing ETS as a Toxic Air Contaminant in January 2006. As part of the assessment, studies on the association between exposure to ETS and breast cancer were reviewed. METHODS: Twenty-six published reports (including 3 meta-analyses) evaluating the association between ETS exposure and breast cancer were reviewed. A weight-of-evidence approach was applied to evaluate the data and draw conclusions about the association between breast cancer and ETS exposure. RESULTS: The published data indicate an association between ETS and breast cancer in younger primarily premenopausal women. Thirteen of 14 studies (10 case-control and four cohort) that allowed analysis by menopausal status reported elevated risk estimates for breast cancer in premenopausal women, seven of which were statistically significant. Our meta-analyses indicated elevated summary relative risks ranging from OR 1.68 (95% C.I. 1.31, 2.15) for all 14 studies to 2.20 (95% C.I. 1.69, 2.87) for those with the best exposure assessment. CONCLUSIONS: Cal/EPA concluded that regular ETS exposure is causally related to breast cancer diagnosed in younger, primarily premenopausal women and that the association is not likely explained by bias or confounding.