Towards a viscoelastic model for the unfused midpalatal suture: development and validation using the midsagittal suture in New Zealand white rabbits.

Maxillary expansion treatment is a commonly used procedure by orthodontists to widen a patient's upper jaw. As this is typically performed in adolescent patients, the midpalatal suture, connective tissue adjoining the two maxilla halves, remains unfused. Studies that have investigated patient response to expansion treatment, generally through finite element analysis, have considered this suture to behave in a linear elastic manner or it was left vacant. The purpose of the study presented here was to develop a model that could represent the midpalatal suture's viscoelastic behavior. Quasilinear viscoelastic, modified superposition, Schapery's, and Burgers modeling approaches were all considered. Raw data from a previously published study using New Zealand White Rabbits was utilized for model parameter estimation and validation. In this study, Sentalloy(®) coil springs at load levels of 0.49N (50g), 0.98N (100g), and 1.96N (200g) were used to widen the midsagittal suture of live rabbits over a period of 6 weeks. Evaluation was based on a models ability to represent experimental data well over all three load sets. Ideally, a single set of model constants could be used to represent data over all loads tested. Upon completion of the analysis it was found that the modified superposition method was able to replicate experimental data within one standard deviation of the means using a single set of constants for all loads. Future work should focus on model improvement as well as prediction of treatment outcomes.

Obesity, waist size and prevalence of current asthma in the California Teachers Study cohort.

BACKGROUND: Obesity is a risk factor for asthma, particularly in women, but few cohort studies have evaluated abdominal obesity which reflects metabolic differences in visceral fat known to influence systemic inflammation. A study was undertaken to examine the relationship between the prevalence of asthma and measures of abdominal obesity and adult weight gain in addition to body mass index (BMI) in a large cohort of female teachers. METHODS: Prevalence odds ratios (ORs) for current asthma were calculated using multivariable linear modelling, adjusting for age, smoking and race/ethnicity. RESULTS: Of the 88 304 women in the analyses, 13% (n = 11,500) were obese (BMI > or = 30 kg/m(2)) at baseline; 1334 were extremely obese (BMI > or = 40 kg/m(2)). Compared with those of normal weight, the adjusted OR for adult-onset asthma increased from 1.40 (95% confidence interval (CI) 1.31 to 1.49) for overweight women to 3.30 (95% CI 2.85 to 3.82) for extremely obese women. Large waist circumference (>88 cm) was associated with increased asthma prevalence, even among women with a normal BMI (OR 1.37, 95% CI 1.18 to 1.59). Among obese women the OR for asthma was greater in those who were also abdominally obese than in women whose waist was < or = 88 cm (2.36 vs 1.57). Obese and overweight women were at greater risk of severe asthma episodes, measured by urgent medical visits and hospital admissions. CONCLUSIONS: This study confirms the association between excess weight and asthma severity and prevalence, and showed that a large waist was associated with increased asthma prevalence even among women considered to have normal body weight.

Fungi and pollen exposure in the first months of life and risk of early childhood wheezing.

BACKGROUND: Many studies have found that the risk of childhood asthma varies by month of birth, but few have examined ambient aeroallergens as an explanatory factor. A study was undertaken to examine whether birth during seasons of elevated ambient fungal spore or pollen concentrations is associated with risk of early wheezing or blood levels of Th1 and Th2 type cells at 24 months of age. METHODS: 514 children were enrolled before birth and followed to 24 months of age. Early wheezing was determined from medical records, and Th1 and Th2 type cells were measured in peripheral blood using flow cytometry. Ambient aeroallergen concentrations were measured throughout the study period and discrete seasons of high spore and pollen concentrations were defined. RESULTS: A seasonal pattern was observed, with birth in autumn to winter (the spore season) associated with increased odds of early wheezing (adjusted odds ratio 3.1; 95% confidence interval 1.3 to 7.4). Increasing mean daily concentrations of basidiospores and ascospores in the first 3 months of life were associated with increased odds of wheeze, as were increasing mean daily concentrations of total and specific pollen types. Levels of Th1 cells at age 24 months were positively associated with mean spore concentrations and negatively associated with mean pollen concentrations in the first 3 months of life. CONCLUSIONS: Children with higher exposure to spores and pollen in the first 3 months of life are at increased risk of early wheezing. This association is independent of other seasonal factors including ambient levels of particulate matter of aerodynamic diameter

The relationship of respiratory and cardiovascular hospital admissions to the southern California wildfires of 2003.

OBJECTIVE: There is limited information on the public health impact of wildfires. The relationship of cardiorespiratory hospital admissions (n = 40 856) to wildfire-related particulate matter (PM(2.5)) during catastrophic wildfires in southern California in October 2003 was evaluated. METHODS: Zip code level PM(2.5) concentrations were estimated using spatial interpolations from measured PM(2.5), light extinction, meteorological conditions, and smoke information from MODIS satellite images at 250 m resolution. Generalised estimating equations for Poisson data were used to assess the relationship between daily admissions and PM(2.5), adjusted for weather, fungal spores (associated with asthma), weekend, zip code-level population and sociodemographics. RESULTS: Associations of 2-day average PM(2.5) with respiratory admissions were stronger during than before or after the fires. Average increases of 70 microg/m(3) PM(2.5) during heavy smoke conditions compared with PM(2.5) in the pre-wildfire period were associated with 34% increases in asthma admissions. The strongest wildfire-related PM(2.5) associations were for people ages 65-99 years (10.1% increase per 10 microg/m(3) PM(2.5), 95% CI 3.0% to 17.8%) and ages 0-4 years (8.3%, 95% CI 2.2% to 14.9%) followed by ages 20-64 years (4.1%, 95% CI -0.5% to 9.0%). There were no PM(2.5)-asthma associations in children ages 5-18 years, although their admission rates significantly increased after the fires. Per 10 microg/m(3) wildfire-related PM(2.5), acute bronchitis admissions across all ages increased by 9.6% (95% CI 1.8% to 17.9%), chronic obstructive pulmonary disease admissions for ages 20-64 years by 6.9% (95% CI 0.9% to 13.1%), and pneumonia admissions for ages 5-18 years by 6.4% (95% CI -1.0% to 14.2%). Acute bronchitis and pneumonia admissions also increased after the fires. There was limited evidence of a small impact of wildfire-related PM(2.5) on cardiovascular admissions. CONCLUSIONS: Wildfire-related PM(2.5) led to increased respiratory hospital admissions, especially asthma, suggesting that better preventive measures are required to reduce morbidity among vulnerable populations.

The impact of components of fine particulate matter on cardiovascular mortality in susceptible subpopulations.

BACKGROUND: Several studies have demonstrated associations between daily mortality and ambient particulate matter less than 2.5 microns in diameter (fine particles or PM2.5). Few, however, have examined the relative toxicities of PM2.5 constituents, including elemental carbon and organic carbon (EC and OC, respectively), nitrates and transition metals. There is also little information about whether associations between PM2.5 constituents and mortality are modified by socioeconomic and demographic factors. AIM: To examine associations of daily cardiovascular mortality with PM2.5 and its constituents after stratification by gender, race/ethnicity and education, using data from six California counties during 2000 to 2003. METHODS: The association of daily counts of cardiovascular mortality with PM2.5 components was analysed using time-series regression analyses. Poisson models with natural splines were used to control for time-varying covariates such as season and weather. Separate models were run after stratification by gender, race/ethnicity (White, Hispanic, Black) and education (high school graduation or not). Models were run for each county and results were combined using random effects meta-analysis. RESULTS: Daily counts of cardiovascular mortality were associated with PM2.5 and several of its species including EC, OC, nitrates, sulphates, potassium, copper and iron. For many of these species, there were significantly higher effect estimates among those with lower educational attainment and Hispanic individuals. For example, while essentially no association was observed for individuals who graduated from high school, an interquartile change in several of the components of PM2.5 was associated with a 3-5% increase in daily mortality among non-high school graduates. CONCLUSION: There is evidence that several PM2.5 constituents may represent important contributors to cardiovascular mortality. Many of these constituents are generated by motor vehicles, especially those with diesel engines, and by residential wood combustion. In addition, factors associated with low educational attainment may increase susceptibility to PM2.5 and its components.

Evidence for the homeostatic regulation of induced beta cell mass expansion.

AIMS/HYPOTHESIS: Diabetes results from an insufficient insulin-secreting beta cell mass. Restoration of beta cell mass through pharmaceutically induced endogenous beta cell mass expansion may revolutionise diabetes therapy. However, it remains to be determined whether the induced beta cell mass expansion is under homeostatic regulation. METHODS: Beta cell mass expansion rates were derived from three separate studies of continuous stimulation of islet neogenesis, including the partial duct obstruction of euglycaemic Syrian hamsters, administration of a pentadecapeptide with the same amino acid sequence as residues 104-118 of islet neogenesis-associated protein (INGAP(104-118)) to euglycaemic Syrian hamsters, as well as to euglycaemic CD-1 mice. The incidence of islet neogenesis, average beta cell size, and beta cell replication and apoptotic rates were determined. RESULTS: Partial duct obstruction led to a approximately 2.5-fold increase in endocrine tissue at day 56 (p<0.05). From day 0 to day 7 the average rate of change of islet area was 12.7% per day, and this rate decreased to 5.3% per day from day 7 to day 42, and to 2.8% per day from day 42 to day 56. Administration of INGAP(104-118) to adult hamsters led to a 31% increase in total beta cell mass at day 30 (p=0.031). From day 0 to day 10 the average rate of beta cell mass expansion was 148 mug/day, whereas from day 10 to day 30 it decreased to 45 mug/day. INGAP(104-118) administration to adult CD-1 mice resulted in an approximately twofold increase in beta cell mass after 31 days (p=0.021). However, at day 90, there was no significant difference vs age-matched control mice (p=0.30), even though the neogenic beta cell mass was approximately fourfold greater (p=0.026). Beta cell replication was decreased by 56% (p<0.048), whereas beta cell apoptosis was fourfold greater (p<0.003) in 90-day INGAP(104-118)-treated mice compared with age-matched control mice. CONCLUSIONS/INTERPRETATION: These data indicate that in the presence of ongoing islet neogenesis, homeostatic regulatory mechanisms intervene to regulate beta cell mass according to the prevailing metabolic requirements.

Autocrine insulin action activates Akt and increases survival of isolated human islets.

AIMS/HYPOTHESIS: The phosphatidylinositol 3-kinase (PI3K)/Akt pathway plays a critical role in promoting the survival of pancreatic beta cells. Akt becomes activated in isolated human islets following overnight culture despite significant levels of cell death. The aim of the current study was to identify the cause of the observed increase in Akt phosphorylation in isolated islets. We hypothesised that a factor secreted by the islets in culture was acting in an autocrine manner to activate Akt. METHODS: In order to identify the stimulus of the PI3K/Akt pathway in culture, we examined the effects of different culture conditions on Akt phosphorylation and islet survival during the immediate post-isolation period. RESULTS: We demonstrated that islet-conditioned medium induced Akt phosphorylation in freshly isolated human islets, whereas frequent medium replacement decreased Akt phosphorylation. Following overnight culture, islet-conditioned medium contained significantly elevated levels of insulin, indicating that insulin may be responsible for the observed increase in Akt phosphorylation. Indeed, treatment with an anti-insulin antibody or with inhibitors of insulin receptor/IGF receptor 1 kinase activity suppressed Akt phosphorylation, leading to decreased islet survival. In addition, dispersion of islets into single cells also suppressed Akt phosphorylation and induced islet cell death, indicating that islet integrity is also required for maximal Akt phosphorylation. CONCLUSIONS/INTERPRETATION: Our findings demonstrate that insulin acts in an autocrine manner to activate Akt and mediate the survival of isolated human islets. These findings provide new information on how culturing islets prior to transplantation may be beneficial to their survival by allowing for autocrine activation of the pro-survival Akt pathway.

Morphogenetic plasticity of adult human pancreatic islets of Langerhans.

The aim of this study was to investigate the phenotypic plasticity of pancreatic islets of Langerhans. Quiescent adult human islets were induced to undergo a phenotypic switch to highly proliferative duct-like structures in a process characterized by a loss of expression of islet-specific hormones and transcription factors as well as a temporally related rise in the expression of markers of both duct epithelial and progenitor cells. Short-term treatment of these primitive duct-like structures with the neogenic factor islet neogenesis-associated protein (INGAP104-118) induced their reconversion back to islet-like structures in a PI3-kinase-dependent manner. These neoislets resembled freshly isolated human islets with respect to the presence and topological arrangement of the four endocrine cell types, islet gene expression and hormone production, insulin content and glucose-responsive insulin secretion. Our results suggest that adult human islets possess a remarkable degree of morphogenetic plasticity. This novel observation may have important implications for understanding pancreatic carcinogenesis and islet neogenesis.

Signals for death and differentiation: a two-step mechanism for in vitro transformation of adult islets of Langerhans to duct epithelial structures.

Phenotypic change of adult pancreatic islets has been implicated in the development of certain pancreatic cancers and in islet transplant failure. The aim of this study was to characterize intracellular events that mediate changes in adult islet phenotype. Using an in vitro islet-to-duct transformation model, canine islets were induced to undergo phenotypic transformation to duct-like epithelial structures through a two-stage process. Stage one was characterized by widespread islet cell apoptosis associated with the formation of cavitary spaces within the islets. During this stage, c-Jun N-terminal regulated kinase (JNK) and caspase-3 activities were elevated, while extracellular signal-regulated kinase (ERK) and Akt activities were decreased. The second stage of the process was characterized by an inversion in the balance in activity between these signal transduction pathways and by a concomitant decrease in apoptosis. The transformed islets were no longer immunoreactive for islet cell hormones, but expressed the duct epithelial cell marker CK-AE1/AE3. In contrast to islet cells, these duct epithelial cells were highly proliferative. To clarify the role of the identified changes in signal transduction events, we performed additional studies using pharmacological inhibitors of enzyme activity and demonstrated that inhibition of JNK and caspase-3 activity prevented cystic transformation. Our results indicate that the balance in signaling activity between ERK/Akt and JNK/caspase-3 appears to be an important regulator of islet cell death and differentiation.

Air pollution and exacerbation of asthma in African-American children in Los Angeles.

Significant increases in asthma morbidity and mortality in the United States have occurred since the 1970s, particularly among African-Americans. Exposure to various environmental factors, including air pollutants and allergens, has been suggested as a partial explanation of these trends. To examine relations between several air pollutants and asthma exacerbation in African-Americans, we recruited a panel of 138 children in central Los Angeles. We recorded daily data on respiratory symptoms and medication use for 13 weeks and examined these data in conjunction with data on ozone (O3) nitrogen dioxide (NO2), particulate matter (PM10 and PM2.5), meteorological variables, pollens, and molds. Using generalized estimating equations, we found associations between respiratory symptom occurrence and several environmental factors. For example, new episodes of cough were associated with exposure to PM10 (OR = 1.25; 95% CI = 1.12-1.39; interquartile range [IQR] = 17 microg/m3, 24-hour average), PM2.5 (OR = 1.10; 95% CI = 1.03-1.18; IQR = 30 microg/m3, 12-hour average), NO2, and the molds Cladosporium and Alternaria, but not with exposure to O3 or pollen. The factors PM10 and O3 were associated with the use of extra asthma medication. For this population several bioaerosols and air pollutants had effects that may be clinically significant.

Coarse and fine particles and daily mortality in the Coachella Valley, California: a follow-up study.

Many epidemiological studies provide evidence of an association between ambient particles, measured as PM10, and daily mortality. Most of these studies have been conducted in urban areas where PM10 is highly correlated with and dominated by fine particles less than 2.5 microm in diameter (PM2.5). Fewer studies have investigated impacts associated with the fraction of coarse mode particles (between 2.5 and 10 microm in diameter). In a previous study using data from 1989 through 1992 in the Coachella Valley, a desert resort and retirement area east of Los Angeles, we reported associations between PM10 and several different measures of mortality [Ostro B.D., Hurley S., and Lipsett M.J. Air pollution and daily mortality in the Coachella Valley, California: a study of PM10 dominated by coarse particles. Environ. Res. 1999: 81: 231-238]. In this arid environment, coarse particles of geologic origin are highly correlated with and comprise approximately 60% of PM10, increasing to >90% during wind events. This study was intended to repeat the earlier investigation using 10 years (1989-1998) of daily data on mortality and PM10. The last 2.5 years of data also included daily measures of PM2.5, allowing examination of size-specific impacts. To ensure adequate statistical power, we attempted to develop predictive models for both fine and coarse particles to use in analyses of the full 10-year period. An acceptable fit was found only for coarse particles, which were found to be a cubic function of PM10 (R2 = 0.95). Outcome variables included several measures of daily mortality, including all-cause (minus accidents and homicides), cardiovascular and respiratory mortality. Multivariate Poisson regression analyses using generalized additive models were employed to explain the variation in these endpoints, controlling for temperature, humidity, day of the week, season, and time, using locally weighted smoothing techniques. Pollution lags of up to 4 days were examined. Several pollutants were associated with all-cause mortality, including PM2.5, carbon monoxide and nitrogen dioxide. More consistent results were found for cardiovascular-specific mortality, for which associations were found for coarse particles (RR = 1.02; 95% C.I., 1.01-1.04), PM10 (RR = 1.03; 95% C.I., 1.01-1.05). None of the pollutants was associated with respiratory-specific mortality. Ozone was not associated with any of the mortality outcomes. These findings are generally consistent with those we previously reported for the Coachella Valley for the period 1989-1992, demonstrating associations between several measures of particulate matter and daily mortality in an environment in which particulate concentrations are dominated by the coarse fraction.

[Air pollution from traffic and the risk of tumors]. / Inquinamento atmosferico da traffico e rischio di tumori.

This paper describes the epidemiological evidence on lung cancer and childhood leukemia in relation to traffic-related air pollution, with particular reference to diesel exhausts, polycyclic aromatic hydrocarbons (PAH) and benzene. Recent epidemiological studies strengthen the hypothesis of an increased lung cancer risk related to residential exposure to air pollution and to occupational exposure to diesel exhausts. The evidence on the carcinogenicity of several PAH mixtures comes from occupational studies, while the risk incurred by the general population is difficult to estimate. A few papers suggest that traffic-related air pollution may be associated with an increased risk of childhood leukemia. The observed relative risks are small but the exposure is widespread. Therefore, the overall impact of exposure to current levels of urban air pollution may be substantial.

Air pollution and daily mortality in the Coachella Valley, California: a study of PM10 dominated by coarse particles.

Many epidemiological studies provide evidence of an association between airborne particles, measured as PM10 (particulate matter less than 10 microm in diameter), and daily morbidity and mortality. Most of these studies have been conducted in urban areas where PM10 consists primarily of fine particles (<2.5 microm in diameter). Few studies have investigated impacts associated with coarse mode particles (>2.5 microm in diameter). We investigated associations between PM10 and daily mortality in the Coachella Valley, a desert resort and retirement area east of Los Angeles, where coarse particles of geologic origin typically comprise approximately 50-60% of PM10 and can exceed 90% during wind events. Our analysis utilized daily data on mortality from 1989 through 1992 as well as several pollutant and meteorological variables, including PM10, nitrates, sulfates, ozone, nitrogen dioxide, carbon monoxide, temperature, and relative humidity. Outcome variables included several measures of daily mortality, including all-cause, cardiovascular and respiratory mortality, and counts of deaths for those above age 50. Multivariate Poisson regression models were used to explain these health endpoints, controlling for temperature, humidity, day of the week, season, and time, using locally weighted smoothing techniques. The analysis indicated statistically significant associations between PM10 (2- or 3-day lags) and each measure of mortality. The results were robust to various model specifications, correction for autocorrelation and overdispersion, and analysis of influential observations. A 10 microg/m3 change in daily PM10 was associated with an approximately 1% increase in mortality, which is of similar magnitude to particle-associated impacts identified in urban areas. Thus, our findings provide evidence for a mortality effect of PM10 in an area where the particulate mass is dominated by coarse particles.

Occupational exposure to diesel exhaust and lung cancer: a meta-analysis.

OBJECTIVES: We undertook a meta-analysis of epidemiological studies investigating the relationship between occupational diesel exhaust exposure and lung cancer. METHODS: Thirty of 47 studies initially identified as potentially relevant met specified inclusion criteria. We extracted or calculated 39 independent estimates of relative risk and derived pooled estimates of risk for all studies and for numerous study subsets by using a random-effects model. We also examined interstudy heterogeneity by using linear metaregressions. RESULTS: There was substantial heterogeneity in the pooled risk estimates for all studies combined and for most subsets. Several factors consistent with higher study quality, however, contributed to increased pooled estimates of risk and lower heterogeneity, including (1) adjustment for confounding by cigarette smoking and other covariates, (2) having a lower likelihood of selection bias, and (3) having increased study power. CONCLUSION: This analysis provides quantitative support for prior qualitative reviews that have ascribed an etiologic role to occupational diesel exhaust exposure in lung cancer induction. Among study populations most likely to have had substantial exposure to diesel exhaust, the pooled smoking-adjusted relative risk was 1.47 (95% confidence interval = 1.29, 1.67).

Air pollution and emergency room visits for asthma in Santa Clara County, California.

During the winters of 1986-1987 through 1991-1992, rainfall throughout much of Northern California was subnormal, resulting in intermittent accumulation of air pollution, much of which was attributable to residential wood combustion (RWC). This investigation examined whether there was a relationship between ambient air pollution in Santa Clara County, California and emergency room visits for asthma during the winters of 1988-1989 through 1991-1992. Emergency room (ER) records from three acute-care hospitals were abstracted to compile daily visits for asthma and a control diagnosis (gastroenteritis) for 3-month periods during each winter. Air monitoring data included daily coefficient of haze (COH) and every-other-day particulate matter with aerodynamic diameter equal to or less than 10 microns (PM10, 24-hr average), as well as hourly nitrogen dioxide and ozone concentrations. Daily COH measurements were used to predict values for missing days of PM10 to develop a complete PM10 time series. Daily data were also obtained for temperature, precipitation, and relative humidity. In time-series analyses using Poisson regression, consistent relationships were found between ER visits for asthma and PM10. Same-day nitrogen dioxide concentrations were also associated with asthma ER visits, while ozone was not. Because there was a significant interaction between PM10 and minimum temperature in this data set, estimates of relative risks (RRs) for PM10-associated asthma ER visits were temperature-dependent. A 60 micrograms/m3 change in PM10 (2-day lag) corresponded to RRs of 1.43 (95% CI = 1.18-1.69) at 20 degrees F, representing the low end of the temperature distribution, 1.27 (95% CI = 1.13-1.42) at 30 degrees F, and 1.11 (95% CI = 1.03-1.19) at 41 degrees F, the mean of the observed minimum temperature. ER visits for gastroenteritis were not significantly associated with any pollutant variable. Several sensitivity analyses, including the use of robust regressions and of nonparametric methods for fitting time trends and temperature effects in the data, supported these findings. These results demonstrate an association between ambient wintertime PM10 and exacerbations of asthma in an area where one of the principal sources of PM10 is RWC.

Indoor air pollution and asthma. Results from a panel study.

Although there is abundant clinical evidence of asthmatic responses to indoor aeroallergens, the symptomatic impacts of other common indoor air pollutants from gas stoves, fireplaces, and environmental tobacco smoke have been less well characterized. These combustion sources produce a complex mixture of pollutants, many of which are respiratory irritants. We report here results of an analysis of associations between indoor pollution and several outcomes of respiratory morbidity in a population of adult asthmatics residing in the Denver, Colorado, metropolitan area. A panel of 164 asthmatics recorded in a daily diary the occurrence of several respiratory symptoms, nocturnal asthma, medication use, and restrictions in activity, as well as the use of gas stoves, wood stoves, or fireplaces, and exposure to environmental tobacco smoke. Multiple logistic regression analysis suggests that the indoor sources of combustion have a statistically significant association with exacerbations of asthma. For example, after correcting for repeated measures and autocorrelation, the reported use of a gas stove was associated with moderate or worse shortness of breath (OR, 1.60; 95% CI, 1.11-2.32), moderate or worse cough (OR, 1.71; 95% CI, 0.97-3.01), nocturnal asthma (OR, 1.01; 95% CI, 0.91-1.13), and restrictions in activity (OR, 1.47; 95% CI, 1.0-2.16). Among this panel of relatively moderate to severe asthmatics, the respiratory irritants produced by several domestic combustion sources were associated with increased morbidity.

The respiratory health impact of a large urban fire.

OBJECTIVES: In July 1988, a fire destroyed a huge supermarket warehouse in Richmond, Calif, sending smoke into residential neighborhoods for nearly a week. There was no organized public health response. To evaluate the respiratory health impact on the general population, a survey of emergency room visits and hospital admissions to the two acute-care hospitals serving the population downwind was conducted. METHODS: Medical records of 489 patients meeting specified diagnostic criteria during the week of the fire and several reference periods were abstracted. Ratios of proportions for respiratory diagnoses (i.e., emergency room visits for a given diagnosis/total emergency room visits) were calculated, comparing the fire week with the reference periods, and 1988 mortality data for the area were reviewed. RESULTS: Ratios of proportions for emergency room visits for asthma and all lower respiratory conditions increased significantly during the fire. Respiratory-related hospitalizations also increased. However, there was no observable increase in respiratory mortality. CONCLUSIONS: This fire was found to have had a moderate impact on the respiratory health of local residents. Public health intervention is indicated to prevent respiratory morbidity when extended exposure to structural fire smoke is predictable.

Air pollution and respiratory morbidity among adults in southern California.

This paper reports the results of an investigation of the acute effects of air pollution in 321 nonsmoking adults residing in Southern California. Previous epidemiologic investigations of effects of acute exposure to ozone have focused on groups who may not be representative of the general public, such as asthmatics or student nurses. For this study, participants recorded the daily incidence of several respiratory symptoms over a 6-month period between 1978 and 1979. The authors examined the impact of ambient concentrations of ozone, particulate sulfates, and other air pollutants on the incidence of respiratory morbidity, measured as either upper or lower respiratory tract symptoms. Using a logistic regression model, the authors found a significant association between the incidence of lower respiratory tract symptoms and 1-hour daily maximum ozone levels (odds ratio (OR) = 1.22, 95% confidence interval (Cl) 1.11-1.34, for a 10 parts per hundred million (pphm) change), 7-hour average ozone levels (OR = 1.32, 95% Cl 1.14-1.52), and ambient sulfates (OR = 1.30, 95% Cl 1.09-1.54, for a 10-micrograms/m3 change), but no association was found with coefficient of haze, a more general measure of particulates. The existence of a gas stove in the home was also associated with lower respiratory tract symptoms (OR = 1.23, 95% Cl 1.03-1.47). The effects of ozone were greater in the subpopulation without a residential air conditioner. In addition, ozone appears to have had a greater effect among individuals with a preexisting respiratory infection.

Synergism between occupational arsenic exposure and smoking in the induction of lung cancer.

We assembled data from numerous studies to examine whether active smoking and occupational exposure to arsenic act synergistically (more than additively) to increase the risk of lung cancer. Although several smaller studies lacked the power to reject simple additive relations, the joint effect from both exposures consistently exceeded the sum of the separate effects by about 70 to 130%. The only study not showing a greater than additive effect appeared to have inadequate data to address this question. We calculated the excess fractions for the synergism; these showed that a minimum of between 30% and 54% of lung cancer cases among those with both exposures could not be attributed to either one or the other exposure alone. Previous authors addressing the synergism between arsenic exposure and smoking have evaluated deviations from a multiplicative model, which is inappropriate for this purpose. Reports of no interaction or "negative" interaction have therefore been misleading. Taken as a whole, the evidence is compelling that arsenic and smoking act in a synergistic manner to produce lung cancer. Substantial reductions in the lung cancer burden of smokers occupationally exposed to arsenic could be achieved by reductions in either exposure. The mechanism for the synergism is unclear.

Asthmatic responses to airborne acid aerosols.

BACKGROUND: Controlled exposure studies suggest that asthmatics may be more sensitive to the respiratory effects of acidic aerosols than individuals without asthma. This study investigates whether acidic aerosols and other air pollutants are associated with respiratory symptoms in free-living asthmatics. METHODS: Daily concentrations of hydrogen ion (H+), nitric acid, fine particulates, sulfates and nitrates were obtained during an intensive air monitoring effort in Denver, Colorado, in the winter of 1987-88. A panel of 207 asthmatics recorded respiratory symptoms, frequency of medication use, and related information in daily diaries. We used a multiple regression time-series model to analyze which air pollutants, if any, were associated with health outcomes reported by study participants. RESULTS: Airborne H+ was found to be significantly associated with several indicators of asthma status, including moderate or severe cough and shortness of breath. Cough was also associated with fine particulates, and shortness of breath with sulfates. Incorporating the participants' time spent outside and exercise intensity into the daily measure of exposure strengthened the association between these pollutants and asthmatic symptoms. Nitric acid and nitrates were not significantly associated with any respiratory symptom analyzed. CONCLUSIONS: In this population of asthmatics, several outdoor air pollutants, particularly airborne acidity, were associated with daily respiratory symptoms.