Biomedical subjects

D R Gold

Publications and source records attributed to D R Gold.

At least 19 recordsLinked to original sources

PubMed2006

Air pollution and inflammation in type 2 diabetes: a mechanism for susceptibility.

BACKGROUND: Particulate air pollution has been associated with several adverse cardiovascular health outcomes, and people with diabetes may be especially vulnerable. One potential pathway is inflammation and endothelial dysfunction-processes in which cell adhesion molecules and inflammatory markers play important roles. AIM: To examine whether plasma levels of soluble intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and von Willebrand factor (vWF) were associated with particle exposure in 92 Boston area residents with type 2 diabetes. METHODS: Daily average ambient levels of air pollution (fine particles (PM2.5), black carbon (BC) and sulphates) were measured approximately 500 m from the patient examination site and evaluated for associations with ICAM-1, VCAM-1 and vWF. Linear regressions were fit to plasma levels of ICAM-1, VCAM-1 and vWF, with the particulate pollutant index, apparent temperature, season, age, race, sex, glycosylated haemoglobin, cholesterol, smoking history and body mass index as predictors. RESULTS: Air pollutant exposure measures showed consistently positive point estimates of association with the inflammatory markers. Among participants not taking statins and those with a history of smoking, associations between PM(2.5), BC and VCAM-1 were particularly strong. CONCLUSIONS: These results corroborate evidence suggesting that inflammatory mechanisms may explain the increased risk of air pollution-associated cardiovascular events among those with diabetes.

Adult↗

PubMed2006

Ambient particulate air pollution and cardiac arrhythmia in a panel of older adults in Steubenville, Ohio.

OBJECTIVES: Ambient particulate air pollution has been associated with increased risk of cardiovascular morbidity and mortality. Pathways by which particles may act involve autonomic nervous system dysfunction or inflammation, which can affect cardiac rate and rhythm. The importance of these pathways may vary by particle component or source. In an eastern US location with significant regional pollution, the authors examined the association of air pollution and odds of cardiac arrhythmia in older adults. METHODS: Thirty two non-smoking older adults were evaluated on a weekly basis for 24 weeks during the summer and autumn of 2000 with a standardised 30 minute protocol that included continuous electrocardiogram measurements. A central ambient monitoring station provided daily concentrations of fine particles (PM(2.5), sulfate, elemental carbon) and gases. Sulfate was used as a marker of regional pollution. The authors used logistic mixed effects regression to examine the odds of having any supraventricular ectopy (SVE) or ventricular ectopy (VE) in association with increases in air pollution for moving average pollutant concentrations up to 10 days before the health assessment. RESULTS: Participant specific mean counts of arrhythmia over the protocol varied between 0.1-363 for SVE and 0-350 for VE. The authors observed odds ratios for having SVE over the length of the protocol of 1.42 (95% CI 0.99 to 2.04), 1.70 (95% CI 1.12 to 2.57), and 1.78 (95% CI 0.95 to 3.35) for 10.0 microg/m3, 4.2 microg/m3, and 14.9 ppb increases in five day moving average PM2.5, sulfate, and ozone concentrations respectively. The other pollutants, including elemental carbon, showed no effect on arrhythmia. Participants reporting cardiovascular conditions (for example, previous myocardial infarction or hypertension) were the most susceptible to pollution induced SVE. The authors found no association of pollution with VE. CONCLUSION: Increased levels of ambient sulfate and ozone may increase the risk of supraventricular arrhythmia in the elderly.

Aged↗

PubMed2005

Fetal cord blood: aspects of heightened immune responses.

Neonatal immune responses have been associated with the development of atopy in childhood. We assessed in cord blood mononuclear cells (CBMC) whether increased allergen/mitogen-induced lymphoproliferation (LP) is associated with pro-allergic Th2 cytokine IL-13 or Th1 cytokine IFN-gamma secretion. We determined whether LP to one allergen is related to heightened lymphocyte function to other allergens/mitogen. CBMC from 135 neonates were stimulated with house dust mite (Derf1), cockroach, ovalbumin, or mitogen. LP to one allergen was associated with significantly increased LP to other allergens/mitogen. Increased Derf1-LP was associated with increased Derf1-induced IL-13 secretion (r = 0.21, p = 0.01). After adjusting for neonatal gender, race, and maternal smoking, Derf1-LP remained associated with Derf1-IL-13 (OR 3.08, 95% CI 1.56-6.10). Increased mitogen-induced proliferation was associated with increased mitogen-induced IL-13 secretion (r = 0.37, p < 0.001). For some individuals, a predisposition to a heightened immune response is already evident at birth. Whether this phenotype results in atopy in childhood warrants further investigation.

Adult↗

PubMed2005

Elevated allergen-induced IL-13 secretion predicts IgE elevation in children ages 2-5 years.

It is unclear if early immune responses to allergens, specifically Th1 and Th2 cytokine production, predict later immune responses, including increased IgE levels. In a group of children (n = 151) with a parental history of allergy or asthma followed from ages 2 through 5 years, we examined IL-13, IL-4, and IFN-gamma secretion by peripheral blood mononuclear cells in response to phytohemagglutinin (PHA), and to dust mite (Der f 1), cockroach (Bla g 2), and cat (Fel d 1) allergens in relation to elevated IgE. Elevated IgE was defined either as a positive IgE-specific response to at least one allergen (dust mite, cockroach, cat, and ovalbumin) or as an elevated total IgE level above a specified cut-off value. In multivariate logistic regression models including 181 observations made between the age of 2 through 5 years and accounting for repeated measures, we found an association between increased IL-13 secretion in response to Der f 1 and elevated IgE (odds ratio [OR] = 1.21, 95% confidence interval [CI] = 1.09-1.34). Age did not modify this relationship. No association was found between allergen-induced IFN-gamma secretion and IgE production. Among the group of children with measurements made at age 4-5 (n = 70), IL-13 in response to Der f 1 (p = 0.046), and IL-4 in response to PHA (p = 0.04) were increased among children with elevated IgE. In a smaller subset of children with measurements made at both age 2-3 and age 4-5 (n = 36), IL-13 levels at age 2-3 were also significantly increased in response to Der f 1 (p = 0.01) and Fel d 1 (p = 0.002) among those with elevated IgE at age 4-5. In a group of children ages 2-5 years, there is an association between IL-13 and elevated IgE.

Allergens↗

PubMed2005

Predictors of indoor exposure to mouse allergen in urban and suburban homes in Boston.

BACKGROUND: Mouse allergen exposure is prevalent among urban children with asthma. Little is known about mouse allergen exposure in children at risk for the development of allergic diseases. AIMS OF THE STUDY: To assess indoor mouse allergen exposure in early life among children with parental history of asthma or allergies. METHODS: Prospective birth cohort study of 498 children with a history of allergy or asthma in at least one parent living in metropolitan Boston. RESULTS: Of the 498 participating children, 357 (71.7%) resided outside the city of Boston and 439 (90.7%) lived in households with incomes > 30,000 dollars. Mouse allergen was detected in 42% of the homes of study participants. In a multivariate analysis adjusting for sex, income, and endotoxin, black race [odds ratio (OR) = 3.0; 95% confidence interval (CI) = 1.3-6.6, P = 0.009], signs of mice in the home at age 2-3 months (OR = 3.0; 95% CI = 1.6-5.6, P = 0.0006), and kitchen cockroach allergen levels > or = 0.05 to < 2 U/g (OR = 1.8; 95% CI = 1.1-3.2, P = 0.02) were associated with detectable mouse allergen in the kitchen. In this model, living in a single detached house was inversely associated with detectable kitchen mouse allergen levels (OR = 0.4; 95% CI = 0.2-0.6, P = 0.0001). CONCLUSION: Infants with a parental history of asthma or allergies are commonly exposed to mouse allergen in their homes. Among infants at high risk for atopy, predictors of increased mouse allergen levels included black race, reported mice exposure, and moderate levels of cockroach allergen.

Air Pollution, Indoor↗

PubMed2005

Traffic related pollution and heart rate variability in a panel of elderly subjects.

BACKGROUND: Particulate air pollution has been associated with increased cardiovascular deaths and hospital admissions. To help understand the mechanisms, the types of particles most involved, and the types of persons most susceptible, the association between exposure to summertime air pollution and heart rate variability (HRV) was examined in a panel study of 28 elderly subjects. METHODS: Subjects were seen once a week for up to 12 weeks and HRV (SDNN, r-MSSD, PNN50, low frequency/high frequency ratio (LFHFR)) was measured for approximately 30 minutes at each session using a defined protocol. Temperature, day of the week, and hour of the day were controlled, and dummy variables for each subject were controlled for subject specific risk factors. RESULTS: PM2.5 was associated with r-MSSD (-10.1% change for an interquartile range (IQR) increase in exposure (95% CI -2.8 to -16.9)) and PNN50, but stronger associations were seen with black carbon, an indicator of traffic particles, which was also associated with SDNN (-4.6% per IQR (95% CI -2.0 to -7.2)) and LFHFR. Secondary particles were more weakly associated with r-MSSD, as was ozone. No associations were seen with SO2 or NO2. CO had similar patterns of association to black carbon, which disappeared after controlling for black carbon. Black carbon had a substantially higher effect on SDNN in subjects who had had a previous myocardial infarction (-12.7%, 95% CI -5.7 to -19.25). CONCLUSIONS: Particles, especially from traffic, are associated with disturbances of autonomic control of the heart.

Aged↗

PubMed2004

Association between air pollution exposure and exhaled nitric oxide in an elderly population.

BACKGROUND: Animal models suggest that the cardiovascular effects of air pollution result in part from inflammation caused by proinflammatory mediators originating in the lung. In a human study of the cardiovascular effects of air pollution, we aimed to evaluate the potential association between air pollution levels and the fraction of exhaled nitric oxide (FE(NO)), a non-invasive measure of airway inflammation. METHODS: Breath samples were collected weekly between September and December 2000 in a community based group of elderly subjects (median age 70.7 years) in Steubenville, Ohio. The samples were analysed for NO. Air pollution levels were measured concurrently at a central site monitor. RESULTS: An increase in the 24 hour average PM(2.5) concentration of 17.7 micro g/m(3) was associated with an increase in FE(NO) of 1.45 ppb (95% CI 0.33 to 2.57) in models adjusted for subject, week of study, day of the week, hour of the day, ambient barometric pressure, temperature, and relative humidity. This represents a change of approximately 15% compared with the mean FE(NO) in the cohort (9.9 ppb). A significant association was also observed for a 24 hour moving average of ambient NO (0.83 ppb increase, 95% CI 0.26 to 1.40). In two-pollutant models, the magnitude and precision of the PM(2.5) effect was not reduced and the ambient NO effect was no longer significant. The associations between FE(NO) and PM(2.5) were significantly higher in subjects with a doctor's diagnosis of COPD (p value for interaction = 0.03). CONCLUSIONS: Ambient pollution may lead to airway inflammation as measured by FE(NO). These subclinical inflammatory changes may be an important step in the pathogenesis of the cardiopulmonary effects induced by exposure to air pollution.

Aged↗

PubMed2003

Dustborne and airborne fungal propagules represent a different spectrum of fungi with differing relations to home characteristics.

BACKGROUND: Exposure to fungi is often assessed by culturing floor dust or air samples. Our objective was to evaluate the relationships between dustborne and airborne fungi and to identify factors that modify these relationships. METHODS: From November 1994 to September 1996 sequential duplicate 45-l air samples were collected in bedrooms of 496 homes in the Boston area, using a Burkard culture plate sampler. After air sampling, bedroom floors were sampled with a vacuum cleaner that was modified to collect dust in a cellulose extraction thimble. Dust was sieved, and the fine dust was dilution-plated onto DG-18 media. RESULTS: Concentrations of total culturable fungi per gram of bedroom-floor dust were correlated weakly, but significantly, with those of indoor air (r = 0.13, P < 0.05). Concentrations of some individual taxa in the dust and indoor air were also weakly associated. Adjusting for the concentrations of fungi in outdoor air, dustborne fungal concentrations were positively associated with those in indoor air for the taxa Cladosporium and Penicillium, but not for total fungi. The indoor air fungal levels were often predicted by different covariates to those predicting fungal levels in dust. The type of housing (house or apartment) and the presence of carpeting were often predictive factors for dust fungi. In contrast, outdoor fungal levels were often predictive of the indoor air fungal levels. CONCLUSIONS: Because our data do not indicate a strong overall relationship between culturable fungi in dust and indoor air, the results from these two methods (dust and air sampling) likely represent different types of potential fungal exposures to residents. It may be essential to collect both air and dust samples, as well as information on housing characteristics, as indicators for fungal exposure.

Air Pollutants↗

PubMed2001

Treatment of mitochondrial cytopathies.

Mitochondrial cytopathies are clinically and biochemically heterogeneous disorders affecting energy production. Because of the diverse symptoms spanning organ systems, the large number of biochemical and genetic defects, and an unpredictable clinical course, there are limited data regarding proven effective therapies. In general, treatments for mitochondrial cytopathies are intended to augment energy production as well as reduce the production of free radicals and other toxic metabolites that further limit the generation of cellular energy. Theoretically, treatment can be aimed at increasing respiratory chain activity by supplementing relative deficiencies of cofactors required for proper functioning. Possible strategies to consider may include dietary management, supplemental vitamins and cofactors, and/or specific medications aimed at a particular symptom.

Education, Medical, Continuing↗

PubMed2001

Exposure to cockroach allergen in the home is associated with incident doctor-diagnosed asthma and recurrent wheezing.

BACKGROUND: Indoor inhaled allergens have been repeatedly demonstrated to worsen asthma in sensitized individuals, but their role in incident asthma is more controversial. OBJECTIVE: We investigated the relationship between exposure to allergens (dust mite, cat, and cockroach) measured in the home and incident doctor-diagnosed asthma and recurrent wheezing in children born to parents with asthma, allergies, or both. METHODS: From an ongoing longitudinal family and birth cohort study, we identified 222 siblings (median age, 2.87 years) of the index children. Allergen levels in the home were measured from dust samples obtained at the beginning of the study. Incident doctor-diagnosed asthma and recurrent wheezing were determined from questionnaires administered at 14 months and 22 months after the initial questionnaire. RESULTS: Thirteen (5.9%) children were reported to have incident asthma, twenty (9.0%) children had recurrent asthmatic wheezing, and 18 (8.1%) had recurrent wheezing without asthma. Compared with children living in homes with Bla g 1 or 2 levels of less than 0.05 U/g, children exposed to Bla g 1 or 2 levels of 0.05 to less than 2 U/g had a relative risk for incident asthma of 8.27 (95% confidence interval, 1.04-66.04), whereas children exposed to Bla g 1 or 2 levels of 2 U/g or greater had a relative risk for incident asthma of 35.87 (95% confidence interval, 4.49-286.62). Cockroach allergen exposure was likewise a significant predictor for recurrent asthmatic wheezing. Neither dust mite nor cat allergen levels were significantly associated with either outcome. These findings remained after control for several covariates. CONCLUSION: Exposure to cockroach allergen early in life may contribute to the development of asthma in susceptible children.

Air Pollution, Indoor↗

PubMed2001

Association of specific allergen sensitization with socioeconomic factors and allergic disease in a population of Boston women.

BACKGROUND: Socioeconomic differences in allergic disease prevalence have been reported; asthma has been associated with poverty in the United States and hay fever and eczema with relative affluence elsewhere. It is not yet established to what degree such differences in disease prevalence reflect patterns of sensitization and specific allergen sensitivities. OBJECTIVE: We analyzed specific and total IgE measurements in a sample of 458 women, enriched for allergic disease, from the metropolitan Boston area to establish the relation of allergen sensitization to markers of socioeconomic status (SES) and to the prevalence and socioeconomic pattern of allergic disease in this community. METHODS: Total and specific IgE antibodies were measured with the UNICAP System; self-reported allergic disease, household income, education, and race-ethnicity were ascertained with a questionnaire; and a further marker of poverty (percentage living below the poverty level) in the women's area of residence was established on the basis of zip codes. Analysis was performed with SAS statistical software. RESULTS: Markers of low SES were univariately associated with increases in total IgE, number of allergen sensitizations, and levels of specific IgE. Socioeconomic differences in sensitization to cockroach (35% vs 6% in the highest and lowest poverty areas), animal (44% vs 26%), and ragweed (49% vs 23%) allergens were most marked. Sensitization primarily to indoor inhalant allergens (not ragweed or ryegrass) were associated with an increased risk of asthma, even after adjustment for SES. CONCLUSION: We have demonstrated a socioeconomic gradient in sensitization that concords with increased rates of asthma in less affluent communities in this population.

Adolescent↗

PubMed2001

House dust endotoxin and wheeze in the first year of life.

We examined endotoxin exposure and wheezing episodes during the first year of life in a birth cohort of 499 infants with one or both parents having a history of asthma or allergy. We measured endotoxin in settled dust from the baby's bed, bedroom floor, family room, and kitchen floor within the first 3 mo after birth. The primary outcomes were any wheeze (versus no wheeze), and repeated wheeze (versus one or no report of wheeze). We found a significant univariate association of elevated endotoxin (> or = 100 EU/ mg) in family room dust with increased risk of any wheeze (Relative Risk = 1.29, 95% CI = 1.03-1.62). The association was not confounded by cockroach allergen, lower respiratory illness (croup, bronchitis, bronchiolitis, and pneumonia), smoking during pregnancy, lower birth weight, maternal asthma, presence of dog, and race/ethnicity in a multivariate model; the multivariate relative risk (RR = 1.33) was marginally significant (95% CI: 1.00-1.76, p < 0.05). In a multivariate model, controlling for the above covariates, elevated endotoxin in family room dust was significantly associated with increased risk (RR = 1.56, 95% CI = 1.03-2.38) of repeated wheeze. These results suggest that home endotoxin exposure may independently increase risk of any wheeze and repeated wheeze during the first year of life for children with a familial predisposition to asthma or allergy.

Allergens↗

PubMed2001

Acute exposure to environmental tobacco smoke and heart rate variability.

Environmental tobacco smoke (ETS) has been associated with cardiovascular mortality. Pathophysiologic pathways leading from ETS exposure to cardiopulmonary disease are still being explored. Reduced cardiac autonomic function, as measured by heart rate variability (HRV), has been associated with cardiac vulnerability and may represent an important pathophysiologic mechanism linking ETS and risk of cardiac mortality. In this study we evaluated acute ETS exposure in a commercial airport with changes in HRV in 16 adult nonsmokers. We conducted ambulatory electrocardiographic (ECG) monitoring for 8-hr periods while participants alternated 2 hr in nonsmoking and smoking areas. Nicotine and respirable suspended particle concentrations and participants' blood oxygen saturation were also monitored. We calculated time and frequency domain measures of HRV for periods in and out of the smoking area, and we evaluated associations with ETS using comparative statistics and regression modeling. ETS exposure was negatively associated with all measures of HRV. During exposure periods, we observed an average decrement of approximately 12% in the standard deviation of all normal-to-normal heart beat intervals (an estimate of overall HRV). ETS exposures were not associated with mean heart rate or blood oxygen saturation. Altered cardiac autonomic function, assessed by decrements in HRV, is associated with acute exposure to ETS and may be part of the pathophysiologic mechanisms linking ETS exposure and increased cardiac vulnerability.

Adult↗

PubMed2001

Predictors of airborne endotoxin in the home.

We identified home characteristics associated with the level of airborne endotoxin in 111 Boston-area homes enrolled in a cohort study of home exposures and childhood asthma, and we developed a predictive model to estimate airborne endotoxin. We measured endotoxin in family-room air and in dust from the baby's bed, family room, bedroom, and kitchen floor. Level of airborne endotoxin was weakly correlated (r < 0.3) with level of endotoxin in each of the four types of dust samples and was significantly correlated with endotoxin in family-room dust (p < 0.05). Endotoxin in family-room dust accounted for < 6% of the variability of airborne endotoxin. In a multivariate model, certain home characteristics were positively (p < 0.05) associated with airborne endotoxin. These included current presence of dog (difference in level, dog vs. no dog = 72%, partial R(2 )= 12.8%), past presence of dog (partial R(2) = 5.5%), and endotoxin level in family-room dust (partial R(2) = 5.3%). Use of a dehumidifier (partial R(2) = 6.4%) was negatively associated (p = 0.02; difference = -31%) with airborne endotoxin. Other home characteristics were identified as important determinants of increased airborne endotoxin in this model, but individual coefficients were not statistically significant (alpha = 0.05): total amount of fine dust collected in the home (partial R(2 )= 3.8%), concrete floor in family room (3.7%), water damage (3.6%), and use of cool-mist humidifier in past year (2.7%). This multivariate model explained 42% of the variability of airborne endotoxin levels, a substantial improvement over that with dust endotoxin alone. Airborne endotoxin in Boston-area homes appears to be determined by the presence of dogs, moisture sources, and increased amounts of settled dust.

Air Pollutants↗

PubMed2001

Mitochondrial cytopathy in adults: what we know so far.

Mitochondrial cytopathies are a diverse group of inherited and acquired disorders that result in inadequate energy production. They can be caused by inheritable genetic mutations, acquired somatic mutations, exposure to toxins (including some prescription medications), and the aging process itself. In addition, a number of well-described diseases can decrease mitochondrial energy production; these include hyperthyroidism, hypothyroidism, and hyperlipidemia.

Adenosine Triphosphate↗

PubMed2000

Ambient pollution and heart rate variability.

BACKGROUND: We investigated associations between ambient pollution levels and cardiovascular function in a repeated measures study including 163 observations on twenty-one 53- to 87-year-old active Boston residents observed up to 12 times from June to September 1997. Particles with aerodynamic diameter </=2.5 microm (PM(2.5)) were measured continuously using a tapered element oscillating microbalance. METHODS AND RESULTS: The protocol involved 25 minutes per week of continuous Holter ECG monitoring, including 5 minutes of rest, 5 minutes of standing, 5 minutes of exercise outdoors, 5 minutes of recovery, and 20 cycles of slow breathing. Heart rate variability (HRV) was assessed through time domain variables: the standard deviation of normal RR intervals (SDNN) and the square root of the mean of the squared differences between adjacent normal RR intervals (r-MSSD). Mean 4-hour PM(2.5) levels ranged from 3 to 49 microg/m(3); 1-hour ozone levels ranged from 1 to 77 ppb. In multivariate analyses, significantly less HRV (SDNN and r-MSSD) was associated with elevated PM(2.5). During slow breathing, a reduction in r-MSSD of 6.1 ms was associated with an interquartile (14.3 microg/m(3)) increase in PM(2.5) during the hour of and the 3 hours previous to the Holter session (P=0.006). During slow breathing, a multiple pollution model was associated with a reduction in r-MSSD of 5.4 ms (P=0.02) and 5.5 ms (P=0.03) for interquartile changes in PM(2.5) and ozone, respectively, resulting in a combined effect equivalent to a 33% reduction in the mean r-MSSD. CONCLUSIONS: Particle and ozone exposure may decrease vagal tone, resulting in reduced HRV.

Aged↗

PubMed2000

Children at risk for asthma: home allergen levels, lymphocyte proliferation, and wheeze.

BACKGROUND: Allergic asthma is a common childhood disease. Although T-lymphocyte activation plays a critical role in allergic asthma, the environmental factors promoting lymphocyte activation in children are not well defined. OBJECTIVE: In a cohort of children at risk for asthma (n = 114), we determined whether the levels of cockroach (Bla g 1 or 2), house dust mite (Der f 1), and cat allergen (Fel d 1) in the home during infancy was associated with subsequent allergen-specific lymphocyte proliferation in later life. METHODS: Dust samples from multiple sites in the home were collected at 3 months of age and were measured for allergen levels. Serial questionnaires were applied. At a median age of 2 years, PBMCs were isolated and lymphocyte proliferation to the home allergens and PHA was determined. RESULTS: Increased lymphocyte proliferative responses to Bla g 2 were associated with higher home levels of Bla g 1 or 2 (P for trend with kitchen Bla g levels =.011), in analyses adjusting for cold in the past week. Proliferative responses to Der f 1 were higher in homes with family room levels of Der f 1 > or =10 microg/g dust than in homes with Der f 1 <2 microg/g, but differences were not significant in analyses adjusting for cold (P =. 15). Repeated wheeze in the first 2 years of life was associated with increased allergen-specific and PHA proliferative responses. CONCLUSION: Early-life cockroach allergen exposure at 3 months of age predicts allergen-specific lymphocyte proliferative responses at a median of 2 years of age.

Air Pollution, Indoor↗

PubMed2000

Air pollution and incidence of cardiac arrhythmia.

Air pollution episodes have been associated with increased cardiovascular hospital admissions and mortality in time-series studies. We tested the hypothesis that patients with implanted cardioverter defibrillators experience potentially life-threatening arrhythmias after such air pollution episodes. We compared defibrillator discharge interventions among 100 patients with such devices in eastern Massachusetts, according to variations in concentrations of particulate matter, black carbon, and gaseous air pollutants that were measured daily for the years 1995 through 1997. A 26-ppb increase in nitrogen dioxide was associated with increased defibrillator interventions 2 days later (odds ratio = 1.8; 95% confidence interval = 1.1-2.9). Patients with ten or more interventions experienced increased arrhythmias in association with nitrogen dioxide, carbon monoxide, black carbon, and fine particle mass. These results suggest that elevated levels air pollutants are associated with potentially life-threatening arrhythmia leading to therapeutic interventions by an implanted cardioverter defibrillator.

Adult↗