Biomass fuels and health: the gap between global relevance and research activity.
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Biomedical subjects
Publications and source records attributed to Maritta S Jaakkola.
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BACKGROUND: Accumulating evidence suggests that reduced duration of pregnancy predicts increased risk of asthma, but the studies published have been inconsistent. OBJECTIVE: We sought to synthesize the evidence on the relation between preterm delivery and the risk of asthma later in life and to assess differences between the studies as potential sources for heterogeneity of the results. METHODS: We conducted a MEDLINE search (until the end of May 2005). The outcome was asthma. The determinant of interest was preterm delivery defined as a gestational age of less than 37 weeks. RESULTS: We identified 19 articles that provided estimates for the meta-analysis. The summary effect estimates for asthma (fixed-effects odds ratio, 1.074 [95% CI, 1.072-1.075]; heterogeneity P = .000; random-effects odds ratio, 1.366 [95% CI, 1.303-1.432]) showed an increased risk in relation to preterm delivery, with substantial heterogeneity between study-specific estimates. The effect of preterm delivery on asthma was stronger in cross-sectional studies; studies with broad outcome criteria, a small sample size, and a younger study population; and studies conducted in English-speaking populations, outside Europe, and published more recently. In metaregression, adjusting for other determinants, the effect estimate was significantly associated only with the mean age of the study population. CONCLUSIONS: The weight of evidence shows that preterm babies have an increased risk of asthma compared with term babies. CLINICAL IMPLICATIONS: Recognition of prematurity as a determinant of asthma emphasizes the importance of active treatment of physiologic airflow obstruction and a need for special preventive measures against known environmental determinants of asthma in preterm babies.
The authors conducted a population-based incident case-control study to assess the relations between different types of interior surface materials and recent renovations at home and at work and the risk of asthma in adults. The authors systematically recruited all new cases of asthma during a 2.5-year study period (1997-2000) and randomly selected controls from a source population consisting of adults 21-63 years of age living in south Finland. The clinically diagnosed cases consisted of 521 adults with new asthma, and the controls consisted of 932 adults fulfilling eligibility criteria. In logistic regression analysis adjusting for confounding, the risk of asthma was related to the presence of plastic wall materials (adjusted odds ratio (OR) = 2.43, 95% confidence interval (CI): 1.03, 5.75) and wall-to-wall carpet at work (adjusted OR = 1.73, 95% CI: 0.74, 4.09), the latter in particular in the presence of mold problems (adjusted OR = 4.64, 95% CI: 1.11, 19.4). Use of floor-leveling plaster at home during the past 12 months was also a determinant of onset of asthma (adjusted OR = 1.81, 95% CI: 1.06, 3.08). These findings underline the need to consider the health aspects of materials used in floor, wall, and other indoor surfaces.
BACKGROUND: Atopy is known to be important for childhood asthma, but this is to our knowledge the first study on its relation with development of asthma in adulthood. OBJECTIVES: We addressed the role of atopy, measured as total IgE and Phadiatop, and of specific IgE antibodies to mites and molds in development of adult-onset asthma. METHODS: A population-based incident case-control study was conducted in the Pirkanmaa District in Southern Finland. All new clinically diagnosed cases of asthma 21-63 years of age were recruited 1997-2000 in the study district. A random sample of the source population formed the controls. A total of 485 cases and 665 controls provided a serum sample. Diagnosis of asthma was based on demonstration of reversibility in lung function investigations. Subjects with previous asthma were excluded. Phadiatop score and IgE antibodies were analyzed with the UniCAP system. RESULTS: The adjusted odds ratio of asthma increased with total IgE and Phadiatop score in a dose-dependent pattern. IgE antibodies to house dust mite and storage mite were significantly related to an increased risk of asthma. Among molds, increased risk of asthma was seen in relation to IgE antibodies to Aspergillus fumigatus and Cladosporium herbarum. Population attributable fraction due to sensitization to common aeroallergens was 30% (95% CI, 23-41). CONCLUSION: Atopy is a strong determinant of asthma in adulthood. Specific IgE antibodies to mites and some molds are significantly related to increased risk of adult-onset asthma. A considerable fraction of adult asthma could be prevented by measures to reduce atopy.
PURPOSE OF REVIEW: The purpose of this review is to summarize the recent evidence on the effect of cleaning jobs on asthma, based on case reports and series of occupational asthma among cleaners, and epidemiological studies on the relationship between different characteristics of cleaning and asthma risk, as well as to elaborate the evidence on potential occupational exposures responsible for the increased asthma risk observed in cleaners. RECENT FINDINGS: Six recent epidemiologic studies strengthen the evidence that domestic and industrial cleaners are at higher risk of asthma compared with professional employees in Europe and the United States. These studies take into account individual confounders, such as age and cigarette smoking. This finding is supported by case reports and registry-based studies of occupational asthma. The studies and reports have identified some chemicals, such as bleach, as specific causes of asthma. Increased risk of asthma has also been related to some specific job tasks, such as cleaning windows and washing dishes. SUMMARY: Recent studies strengthen the evidence of an increased asthma risk among cleaners or individuals in other jobs in which they are involved in cleaning. Further research should be directed to elaborate how much of asthma is related to specific sensitization to certain chemicals and how much to airway inflammation induced by exposure to a mixture of irritants.
Asthma is a multifactorial airway disease that arises from a relatively common genetic background interphased with exposures to allergens and airborne irritants. The rapid rise in asthma over the past three decades in Western societies has been attributed to numerous diverse factors, including increased awareness of the disease, altered lifestyle and activity patterns, and ill-defined changes in environmental exposures. It is well accepted that persons with asthma are more sensitive than persons without asthma to air pollutants such as cigarette smoke, traffic emissions, and photochemical smog components. It has also been demonstrated that exposure to a mix of allergens and irritants can at times promote the development phase (induction) of the disease. Experimental evidence suggests that complex organic molecules from diesel exhaust may act as allergic adjuvants through the production of oxidative stress in airway cells. It also seems that climate change is increasing the abundance of aeroallergens such as pollen, which may result in greater incidence or severity of allergic diseases. In this review we illustrate how environmental tobacco smoke, outdoor air pollution, and climate change may act as environmental risk factors for the development of asthma and provide mechanistic explanations for how some of these effects can occur.
OBJECTIVES: Despite a heavy burden of HIV/AIDS and other blood borne infections, few studies have investigated needle stick injuries in sub-Saharan Africa. We conducted a cross-sectional study at Mulago national referral hospital in Kampala, Uganda, to assess the occurrence and risk factors of needle stick injuries among nurses and midwives. METHODS: A total of 526 nurses and midwives involved in the direct day-to-day management of patients answered a questionnaire inquiring about occurrence of needle stick injuries and about potential predictors, including work experience, work load, working habits, training, and risk behaviour. RESULTS: A 57% of the nurses and midwives had experienced at least one needle stick injury in the last year. Only 18% had not experienced any such injury in their entire career. The rate of needle stick injuries was 4.2 per person-year. Multiple logistic regression analysis showed that the most important risk factor for needle stick injuries was lack of training on such injuries (OR 5.72, 95% CI 3.41-9.62). Other important risk factors included working for more than 40 h/week (OR 1.90, 95% CI 1.20-3.31), recapping needles most of the time (OR 1.78, 95% CI 1.11-2.86), and not using gloves when handling needles (OR 1.91, 95% CI 1.10-3.32). CONCLUSIONS: The study showed a high rate of needle stick injuries among nurses and midwives working in Uganda. The strongest predictor for needle stick injuries was lack of training. Other important risk factors were related to long working hours, working habits, and experience.
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The present study describes salivary cotinine levels and their relationship to cigarettes smoked per day in Mexican smokers. Using a sampling strategy based on the number of cigarettes per day, we recruited 1,222 smokers from Mexico City and the state of Morelos in Mexico during 1999. Smoking behaviors and other factors known to affect nicotine intake and cotinine level were identified in an interview using a standardized questionnaire. Salivary cotinine was measured by capillary gas chromatography with nitrogen-phosphorus detection. We used generalized additive models to describe the relationship between salivary cotinine levels and variables of interest. The mean age of the population was 39.7 years (SD=15.6 years), with a mean cotinine level of 194.7 ng/ml (SD=134.8; range=10.1-767). Participants smoked a mean of 15.5 cigarettes per day (SD=11.3). Salivary cotinine and cigarettes smoked per day were positively related, although the association was not linear, flattening above 20 cigarettes per day. After adjusting for cigarettes per day, we found that significant predictors of cotinine levels included age, body mass index, cigarette producer, and smoking behavior variables. These results may have implications for dosing with nicotine medications to aid smoking cessation in Mexican smokers and suggest that whether the cigarette is labeled light or regular has no relationship to nicotine dose from smoking cigarettes.
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The authors assessed the relations between occupation and risk of developing asthma in adulthood in a 1997-2000 population-based incident case-control study of 521 cases and 932 controls in south Finland. The occupations were classified according to potential exposure to asthma-causing inhalants. Asthma risk was increased consistently for both men and women in the chemical (adjusted odds ratio (OR) = 5.69, 95% confidence interval (CI): 1.08, 29.8), rubber and plastic (OR = 2.61, 95% CI: 0.92, 7.42), and wood and paper (OR = 1.72, 95% CI: 0.71, 4.17) industries. Risk in relation to occupation was increased only for men-for bakers and food processors (OR = 8.62, 95% CI: 0.86, 86.5), textile workers (OR = 4.70, 95% CI: 0.29, 77.1), electrical and electronic production workers (OR = 2.83, 95% CI: 0.82, 6.93), laboratory technicians (OR = 1.66, 95% CI: 0.17, 16.6), and storage workers (OR = 1.57, 95% CI: 0.40, 6.19). Of the predominantly men's occupations, metal (OR = 4.52, 95% CI: 2.35, 8.70) and forestry (OR = 6.00, 95% CI: 0.96, 37.5) work were the strongest determinants of asthma. For women, asthma risk increased for waiters (OR = 3.03, 95% CI: 1.10, 8.31), cleaners (OR = 1.42, 95% CI: 0.81, 2.48), and dental workers (OR = 4.74, 95% CI: 0.48, 46.5). Results suggest an increased asthma risk both in traditional industries and forestry and in several nonindustrial occupations.
BACKGROUND: Identifying factors that affect cotinine levels in smokers may be useful for smoking cessation programs. Our aims were to characterize the distribution of salivary cotinine levels in Chinese smokers and to investigate factors that influence cotinine concentrations. METHODS: In a cross-sectional study, 600 Chinese adult smokers answered a questionnaire on smoking habits and provided a saliva sample for cotinine analysis. Modification of the relation between number of cigarettes smoked and cotinine concentration by individual characteristics, smoking behavior, and type of tobacco was evaluated. RESULTS: Quadratic model provided the best fit for the relation between number of cigarettes smoked in the previous 24 hours and salivary cotinine concentration. Among those smoking up to 20 cigarettes, the median cotinine concentration was higher among younger subjects, those smoking cigarettes without filter and regular rather than light cigarettes, and those inhaling frequently and deeply. Such trends were not observed among heavier smokers. The increase in cotinine per cigarette tended to be larger in those with lower median cotinine level. CONCLUSIONS: Our findings show that smoking behavior-related factors modify the relation between number of cigarettes smoked and salivary cotinine concentration. This suggests that smokers may regulate their smoking behavior to achieve a certain optimum nicotine level.
AIMS: This study evaluated the possible impact of national smoke-free work-place legislation on employee exposure to environmental tobacco smoke (ETS), employee smoking habits and attitudes on work-place smoking regulations. DESIGN: Repeated cross-sectional questionnaire surveys and indoor air nicotine measurements were carried out before, and 1 and 3 years after the law had come into effect. SETTING: Industrial, service sector and office work-places from the Helsinki metropolitan area, Finland. PARTICIPANTS: A total of 880, 940 and 659 employees (response rates 70%, 75% and 75%) in eight work-places selected from a register kept by the Uusimaa Regional Institute of Occupational Health to represent various sectors of public and private work-places. MEASUREMENTS: Reported exposure to ETS, smoking habits, attitudes on smoking at work and measurements of indoor air nicotine concentration. FINDINGS: Employee exposure to ETS for at least 1 hour daily decreased steadily during the 4-year follow-up, from 51% in 1994 to 17% in 1995 and 12% in 1998. Respondents' daily smoking prevalence and tobacco consumption diminished 1 year after the enforcement of legislation from 30% to 25%, and remained at 25% in the last survey 3 years later. Long-term reduction in smoking was confined to men. Both smokers' and non-smokers' attitudes shifted gradually towards favouring a total ban on smoking at work. Median indoor airborne nicotine concentrations decreased from 0.9 micro g/m3 in 1994-95 to 0.1 micro g/m3 in 1995-96 and 1998. CONCLUSIONS: This is the first follow-up study on a nationally implemented smoke-free work-place law. We found that such legislation is associated with steadily reducing ETS exposure at work, particularly at work-places, where the voluntary smoking regulations have failed to reduce exposure. The implementation of the law also seemed to encourage smokers to accept a non-smoking work-place as the norm.
OBJECTIVES: The authors assessed the effects of environmental tobacco smoke (ETS) on the development of asthma in adults. METHODS: In the Pirkanmaa district of South Finland, all 21- to 63-year-old adults with new cases of asthma diagnosed during a 2.5-year period (n = 521 case patients, out of 441 000 inhabitants) and a random sample of control subjects from the source population (932 control subjects) participated in a population-based incident case-control study. RESULTS: Risk of asthma was related to workplace ETS exposure (adjusted odds ratio [OR] = 2.16; 95% confidence interval [CI] = 1.26, 3.72) and home exposure (OR = 4.77; 95% CI = 1.29, 17.7) in the past year. Cumulative ETS exposure over a lifetime at work and at home increased the risk. CONCLUSIONS: This study indicates for the first time that both cumulative lifetime and recent ETS exposures increase the risk of adult-onset asthma.
BACKGROUND: Studies of exposure to pets and the risk of asthma have provided conflicting results. OBJECTIVE: We conducted a population-based incident case-control study to assess the relationship of current and previous pet keeping with the risk of adult-onset asthma. We also investigated whether genetic propensity as a result of parental atopy modifies these relations. METHODS: From the source population of 441,000 inhabitants of a geographically defined area in South Finland, we systematically recruited, during a 2.5-year period, all new cases of asthma in 21- to 63-year-old adults and randomly selected control subjects. The clinically diagnosed case series consisted of 521 adults with newly diagnosed asthma and a control series of 932 control subjects. Information on current and past exposure to hairy pets was collected by using a self-administered questionnaire. RESULTS: In logistic regression analysis the risk of asthma was lower among subjects with pets during the past 12 months (adjusted odds ratio [OR], 0.74; 95% confidence interval [CI], 0.57-0.96) but higher among subjects with pets more than 12 months previously (adjusted OR, 1.39; 95% CI, 1.05-1.84). Parental atopy increased the risk of asthma (OR, 1.88; 95% CI, 1.47-2.41), but there was no interaction between parental atopy and pet exposure. CONCLUSIONS: The present results are consistent with the hypothesis that both keeping furry pets and parental atopy increase the risk of asthma development in adulthood. Parental atopy does not modify the effects of pet exposure. The negative association between current pets and the risk of asthma is consistent with selective avoidance of these pets by symptomatic individuals.
Previous cross-sectional and prevalent case-control studies have suggested increased risk of asthma in adults related to dampness problems and molds in homes. We conducted a population-based incident case-control study to assess the effects of indoor dampness problems and molds at work and at home on development of asthma in adults. We recruited systematically all new cases of asthma during a 2.5-year study period (1997-2000) and randomly selected controls from a source population consisting of adults 21-63 years old living in the Pirkanmaa Hospital district, South Finland. The clinically diagnosed case series consisted of 521 adults with newly diagnosed asthma and the control series of 932 controls, after we excluded 76 (7.5%) controls with a history of asthma. In logistic regression analysis adjusting for confounders, the risk of asthma was related to the presence of visible mold and/or mold odor in the workplace (odds ratio, 1.54; 95% confidence interval, 1.01-2.32) but not to water damage or damp stains alone. We estimated the fraction of asthma attributable to workplace mold exposure to be 35.1% (95% confidence interval, 1.0-56.9%) among the exposed. Present results provide new evidence of the relation between workplace exposure to indoor molds and adult-onset asthma.
In this paper, current knowledge on the respiratory effects of environmental tobacco smoke among adults is synthesized, and the biological basis and methodological issues are discussed. The Medline database was searched from 1966 through October 2000. All of the related respiratory effects have been linked to both home and workplace exposures. Some evidence of a dose-response relation has also been detected for all respiratory conditions. The strongest evidence of a causal relation exists for chronic respiratory symptoms. Harmful effects on lung function have also been detected, mainly in countries and occupations with high exposure levels. There is limited evidence indicating an increased risk of its causing asthma and chronic obstructive pulmonary disease, and also for poor control of established asthma. More longitudinal studies with careful assessment of exposure are needed for better risk estimates. Despite these challenges for the future, the combination of toxicologic evidence, abundant evidence on respiratory effects among children, and the studies reviewed in this paper point to an urgent need for measures to prevent exposure to environmental tobacco smoke among adults.
This review synthesizes current knowledge of the effects of prenatal and postnatal exposure to environmental tobacco smoke on the respiratory health of children. A Medline database search was conducted for 1966 through October 2000. Limited evidence was found that exposure in pregnancy influences fetal growth, increases the risk of preterm delivery, and predicts the development of asthma and reduced lung function later in life. Both occupational and home environments contribute to the exposure of pregnant women and thus indirectly to adverse effects on children. There is strong and consistent evidence that exposure in childhood causes chronic respiratory symptoms (eg, cough, phlegm, and wheezing) and induces asthma. Limited evidence supports the role of childhood exposure in the poor overall control of established disease. Postnatal exposure is likely to have a small adverse impact on lung function growth. Prenatal and postnatal exposures have an important impact on children's respiratory health. These effects are preventable if pregnant women and children are protected from exposure to environmental tobacco smoke.