Occupation and occurrence of respiratory infections among adults with newly diagnosed asthma.

BACKGROUND: Work environments are potential areas for spreading respiratory infections. We hypothesized that certain occupations increase susceptibility to respiratory infections among adults with asthma. Our objective was to compare the occurrence of respiratory infections among different occupations in adults with newly diagnosed asthma. METHODS: We analysed a study population of 492 working-age adults with newly diagnosed asthma who were living in the geographically defined Pirkanmaa Area in Southern Finland during a population-based Finnish Environment and Asthma Study (FEAS). The determinant of interest was occupation at the time of diagnosis of asthma. We assessed potential relations between occupation and occurrence of both upper and lower respiratory tract infections during the past 12 months. The measures of effect were incidence rate ratio (IRR) and risk ratio (RR) adjusted for age, gender, and smoking habits. Professionals, clerks, and administrative personnel formed the reference group. RESULTS: The mean number of common colds in the study population was 1.85 (95% CI 1.70, 2.00) infections in the last 12 months. The following occupational groups showed increased risk of common colds: forestry and related workers (aIRR 2.20, 95% CI 1.15-4.23) and construction and mining (aIRR 1.67, 95% CI 1.14-2.44). The risk of lower respiratory tract infections was increased in the following groups: glass, ceramic, and mineral workers (aRR 3.82, 95% CI 2.54-5.74), fur and leather workers (aRR 2.06, 95% CI 1.01-4.20) and metal workers (aRR 1.80, 95% CI 1.04-3.10). CONCLUSIONS: We provide evidence that the occurrence of respiratory infections is related to certain occupations.

Effects of occupational exposures on respiratory health in steel factory workers.

Background: The steel factory work environment contains various chemical exposures that can affect indoor air quality and have impact on respiratory health of the workers. Aims: The objective of this study was to assess potential effects of occupational exposures in steel factory workers in Iran on the respiratory symptoms, occurrence and the lung function levels. Method: This was a cross-sectional study of 133 men working in a steel factory forming the exposed group and 133 male office workers forming the reference group from a steel company in Iran. The participants filled in a questionnaire and underwent spirometry. Work history was used both as dichotomous (exposed/reference) and a quantitative measure of exposure, the latter measured as duration of exposure in the specified work (in years) for the exposed group and zero for the reference group. Results: Multiple linear regression and Poisson regression were used to adjust for confounding. In Poisson regression analyses, an increased prevalence ratio (PR) of all respiratory symptoms was observed in the exposed group. Lung function parameters were significantly reduced in the exposed group (p < 0.001). There was a dose-response relation between duration of occupational exposures and reduction in the predicted value of FEV1/FVC level (0.177, 95% CI -0.198 to -0.156) in all models. Conclusion: The results of these analyses showed that occupational exposures in steel factory work increase the prevalence of respiratory symptoms and reduce lung function. Safety training and workplace conditions were found to need improvement. In addition, use of proper personal protective equipment is recommended.

Subtypes of Adult-Onset Asthma at the Time of Diagnosis: A Latent Class Analysis.

INTRODUCTION: Only a few previous studies have investigated the subtypes of adult-onset asthma. No previous study has assessed whether these subtypes are different between men and women, or whether these subtypes have different risk factors. METHODS: We applied latent class analyses to the Finnish Environment and Asthma Study population, including 520 new cases of adult-onset asthma. We formed subtypes separately between women and men and analyzed the following determinants as potential predictors for these subtypes: age, body mass index, smoking, and parental asthma. RESULTS: Among women, the subtypes identified were: 1. Moderate asthma, 2. Cough-variant asthma, 3. Eosinophilic asthma, 4. Allergic asthma, and 5. Difficult asthma. Among men, the subtypes were: 1. Mild asthma, 2. Moderate asthma, 3. Allergic asthma, and 4. Difficult asthma. Three of the subtypes were similar among women and men: Moderate, Allergic, and Difficult asthma. In addition, women had two distinct subtypes: Cough-variant asthma, and Eosinophilic asthma. These subtypes had different risk factor profiles, e.g., heredity was important for Eosinophilic and Allergic asthma (RR for Both parents having asthma in Eosinophilic 3.55 (1.09 to 11.62)). Furthermore, smoking increased the risk of Moderate asthma among women (RR for former smoking 2.21 (1.19 to 4.11)) and Difficult asthma among men but had little influence on Allergic or Cough-variant asthma. Conclusion: This is an original investigation of the subtypes of adult-onset asthma identified at the time of diagnosis. These subtypes differ between women and men, and these subtypes have different risk factor profiles. These findings have both clinical and public health importance for the etiology, prognosis, and treatment of adult-onset asthma.

Do hospital workers experience a higher risk of respiratory symptoms and loss of lung function?

BACKGROUND: Hospital work environment contains various biological and chemical exposures that can affect indoor air quality and have impact on respiratory health of the staff. The objective of this study was to investigate potential effects of occupational exposures on the risk of respiratory symptoms and lung function in hospital work, and to evaluate potential interaction between smoking and occupational exposures. METHODS: We conducted a cross-sectional study of 228 staff members in a hospital and 228 employees of an office building as the reference group in Shiraz, Iran. All subjects completed a standardized ATS respiratory questionnaire and performed a spirometry test. RESULTS: In Poisson regression, the adjusted prevalence ratios (aPR) among the hospital staff were elevated for cough (aPR 1.90, 95% CI 1.15, 3.16), phlegm production (aPR 3.21, 95% CI 1.63, 6.32), productive cough (aPR 2.83, 95% CI 1.48, 5.43), wheezing (aPR 3.18, 95% CI 1.04, 9.66), shortness of breath (aPR 1.40, 95% CI 0.93, 2.12), and chest tightness (aPR 1.73, 95% CI 0.73, 4.12). Particularly laboratory personnel experienced increased risks of most symptoms. In linear regression adjusting for confounding, there were no significant differences in lung function between the hospital and office workers. There was an indication of synergism between hospital exposures and current smoking on FEV1/FVC% (interaction term ß = - 5.37, 95% CI - 10.27, - 0.47). CONCLUSIONS: We present significant relations between hospital work, especially in laboratories, and increased risks of respiratory symptoms. Smoking appears to enhance these effects considerably. Our findings suggest that policymakers should implement evidence-based measures to prevent these occupational exposures.

Different effects of smoking on atopic and non-atopic adult-onset asthma.

BACKGROUND: Both tobacco smoking and atopy increase the risk of adult-onset asthma. We studied if there are differences in the effects of smoking on the risks of atopic and non-atopic adult-onset asthma, and if gender modifies these effects. METHODS: The Finnish Environment and Asthma Study (FEAS) includes 521 incident cases of adult-onset asthma and 932 population-based controls, aged 21 to 63 years, recruited from a geographically defined area of Pirkanmaa, South Finland. Asthma was defined based on symptoms and lung function measurements, atopy by IgE antibodies to common aeroallergens and smoking by the study questionnaire. RESULTS: Altogether 212 cases were atopic, and 251 cases were non-atopic. Regular smoking increased the risk of atopic asthma (adjusted OR 1.24, 95% CI 0.83-1.85), this effect was seen in women (aOR 1.77, 1.06-2.95) but not in men (aOR 0.75, 0.39-1.45). Among regular smokers, the amount smoked was lowest among women with atopic asthma. Recent quitting of smoking was related to increased risk of both atopic (aOR 4.91, 2.26-10.65) and non-atopic (aOR 4.37, 1.87-10.21) asthma. Having quitted smoking over a year ago was related to increased risk of non-atopic asthma (aOR 1.57, 1.08-2.28), mainly in men (aOR 2.03, 1.06-3.88). CONCLUSIONS: In women, rather small amounts of regular smoking increase the risk of atopic asthma. However, for non-atopic asthma, the smoking induced risk continues for longer after quitting, especially in men. In conclusion, the effects of smoking on the risks of atopic and non-atopic asthma differ, and gender modifies these effects.

Occupation and subcategories of asthma: a population-based incident case-control study.

BACKGROUND: We hypothesised that occupational exposures differently affect subtypes of adult-onset asthma. OBJECTIVE: We investigated potential relations between occupation and three subtypes of adult asthma, namely atopic asthma, non-atopic asthma and asthma-COPD overlap syndrome (ACOS). METHODS: This is a population-based case-control study of incident asthma among working-age adults living in Pirkanmaa Hospital District in Southern Finland. The determinant of interest was occupation at the time of diagnosis of asthma or the job that the subject had quit due to respiratory symptoms. Asthma was divided into three mutually exclusive subtypes on the basis of any positive IgE antibody (atopic and non-atopic asthma) and presence of persistent airways obstruction in spirometry (ACOS). We applied unconditional logistic regression analysis to estimate adjusted OR (aOR), taking into account gender, age and smoking. RESULTS: The following occupational groups showed significantly increased risk of atopic asthma: chemical industry workers (aOR 15.76, 95% CI 2.64 to 94.12), bakers and food processors (aOR 4.69, 95% CI 1.18 to 18.69), waiters (aOR 4.67, 95% CI 1.40 to 15.56) and those unemployed (aOR 3.06, 95% CI 1.52 to 6.17). The following occupations showed clearly increased risk of non-atopic asthma: metal workers (aOR 8.37, 95% CI 3.77 to 18.59) and farmers and other agricultural workers (aOR 2.36, 95% CI 1.10 to 5.06). Some occupational groups showed statistically significantly increased OR of ACOS: electrical and electronic production workers (aOR 30.6, 95% CI 6.10 to 153.35), fur and leather workers (aOR 16.41, 95% CI 1.25 to 215.85) and those retired (aOR 5.55, 95% CI 1.63 to 18.97). CONCLUSIONS: Our results show that different occupations are associated with different subtypes of adult-onset asthma.

Occupational exposures and respiratory symptoms and lung function among hairdressers in Iran: a cross-sectional study.

OBJECTIVE: Exposures at hairdressers' work have been reported to lead to an increased risk of several health outcomes. The present study aimed to investigate the relations between occupational exposures and respiratory symptoms and lung function among hairdressers in Iran. METHODS: We conducted a cross-sectional study to compare potential respiratory effects among 140 women working as hairdressers to such effects among 140 women working as office workers (administrative personnel). Both groups worked in Shiraz, Iran. Respiratory symptoms were assessed by a standard respiratory questionnaire. The questionnaire also inquired about substances used and workspace conditions, including ventilation type. Lung function levels were measured by spirometry. RESULTS: Respiratory symptoms, including cough, wheezing, shortness of breath, and chest tightness were significantly more frequent in hairdressers compared to the reference group (p < 0.05). After controlling for potential confounders, hairdressers had a prevalence ratio (PR) of 2.18 (95% CI 1.26-3.77) for cough, 9.59 (95% CI 1.004-91.73) for wheezing, 2.06 (95% CI 1.25-3.39) for shortness of breath, and 3.31 (95% CI 1.84-5.97) for chest tightness compared to the reference group. Lung function parameters (including VC, FVC, and FEV1) were significantly reduced in hairdressers (p < 0.001). Absence of air conditioning predicted greater reduction in lung function (p < 0.05) in the exposed. Decrease in FVC with normal FEV1/FVC in the exposed group suggested existence of restrictive lung function. CONCLUSIONS: This study provides evidence of increased prevalence of respiratory symptoms and restrictive lung function impairment among hairdressers in Iran.

Occurrence of respiratory symptoms and lung function deficits among fruit and vegetable market workers.

OBJECTIVE: The objective of this study was to investigate the potential effects of occupational exposures among fruit and vegetable market workers on the occurrence of respiratory symptoms and on the level of lung function parameters. METHODS: We conducted a cross-sectional study of 140 men working as fruit and vegetable market workers (response rate 100%) and a reference group of 77 male office workers as the reference group (response rate 55%) from Shiraz, Iran. The outcomes of interest included occurrence of respiratory symptoms assessed by a standard respiratory questionnaire and lung function assessed by spirometry. RESULTS: In Poisson regression analyses, the exposed group showed increased prevalence ratio (PR) of wheezing (adjusted PR 5.32, 95% CI 1.40 to 20.26), after controlling for confounding. Cough (PR 3.30, 95% CI 1.16 to 9.40) and wheezing (PR 9.40, 95% CI 2.28 to 38.64) showed increased PRs among vegetable distributors. Forced expiratory volume in 1 s (FEV1) and FEV1/forced vital capacity were significantly decreased among exposed workers after controlling for confounders. The absolute value of FEV1 level was reduced significantly among fruit and vegetable carters (-0.99, 95% CI -1.68 to -0.32) and vegetable (-0.51, 95% CI -0.93 to -0.10) and fruit (-0.51, 95% CI -0.86 to -0.15) distributors in comparison with the reference group in the adjusted full model. CONCLUSIONS: This study provides evidence that fruit and vegetable market workers are at an increased risk of respiratory symptoms and reduced lung function. Workplace conditions and safety training clearly need improvement, and there is a likely role for proper use of personal protective equipment.

Indoor mold odor in the workplace increases the risk of Asthma-COPD Overlap Syndrome: a population-based incident case-control study.

BACKGROUND: Previous studies have suggested an increased risk of asthma related to indoor dampness problems, but their role in the etiology of Asthma-COPD Overlap Syndrome has not been studied. We utilized a population-based incident case-control study to assess potential effect of indoor dampness and molds at home and at work on development of ACOS. METHODS: We recruited systematically all new cases of asthma diagnosed during a 2.5-year study period (1997-2000) and randomly selected controls from the source population of adults 21-63 years old and representing 500,000 persons-years in the Pirkanmaa Hospital District, South Finland. Exposure indicators included water damage, damp stains or paint peeling, visible mold, and mold odor, asked separately for home and workplace. The clinically diagnosed case series consisted of 521 adults with newly diagnosed asthma. Altogether 25 of them satisfied the criteria for ACOS-cases, i.e. FEV1/FVC < 0.70 in post-bronchodilator spirometry. The control series, including 932 controls, were from a random sample of source population, after excluding 76 (7.5%) controls with asthma. RESULTS: In logistic regression analysis adjusting for confounders, the risk of ACOS was significantly related to presence of mold odor in the workplace (OR 3.43; 95% CI 1.04-11.29), but not to other dampness indicators. The fraction of ACOS attributable to workplace mold odor was 70.8% (95% CI 3.8-91.1%) among the exposed. The risk of ACOS was not related to mold exposures at home. CONCLUSIONS: Present results provide new evidence of the significant relation between workplace exposure to mold odor and adult-onset ACOS.

Smoking and lung function among adults with newly onset asthma.

Introduction: Smoking increases the risk of asthma and reduces lung function among subjects with and without asthma. We assessed the effects of smoking on lung function reflecting both central and small airways among adults with newly onset asthma. Methods: In a population-based study, 521 (response rate 86%) working-aged adults with clinically defined newly diagnosed asthma answered a questionnaire on personal smoking and other factors potentially influencing lung function, and performed spirometry. We applied multiple linear regression analysis to estimate the relations between smoking and lung function adjusting for confounding. Results: Among asthmatics, FEV1 level was reduced significantly, on average 208 mL, related to regular smoking (adjusted effect estimate -0.208, 95% CI -0.355 to -0.061) and 245 mL in relation to former smoking, that is, among those who quit less than a year ago (-0.245, 95% CI -0.485 to -0.004). In contrast, FEV1 was not significantly related to occasional smoking or former smoking among those who quit over a year ago. Forced expiratory flow (FEF) levels (L/s) were also significantly reduced among regular smokers (FEF25-75%: -0.372, 95% CI -0.607 to -0.137; FEF50%: -0.476, 95% CI -0.750 to -0.202). An exposure-response pattern related to both daily smoking rate and lifetime cumulative smoking was seen both among men and women. Conclusions: This study provides new evidence that among working-aged adults with new asthma, regular smoking and former smoking reduce lung function levels with a dose-response pattern. The lung function parameters applied as outcomes reflect both larger and smaller airways.

The synergistic effect of heredity and exposure to second-hand smoke on adult-onset asthma.

RATIONALE: Identification of the subpopulation especially susceptible to the adverse effects of second-hand smoke exposure (SHS) would be useful for preventive actions and interventions. OBJECTIVES: To investigate whether asthmatic heredity indicates susceptibility to the effects of SHS on the risk of adult-onset asthma. METHODS: A population-based incident case-control study of clinically defined adult-onset asthma and randomly drawn control subjects (adults 21-63 yr old) from a geographically defined area in South Finland. After excluding current and ex-smokers there were 226 cases and 450 disease-free control subjects. MEASUREMENTS AND MAIN RESULTS: Our outcome measure was new adult-onset asthma. Parental asthma and recent SHS had a synergistic effect on the risk of asthma, the adjusted odds ratio being 1.97 (95% confidence interval, 1.12-3.45) for SHS; 2.64 (1.65-4.24) for parental asthma; and 12.69 (3.44-46.91) for their joint effect (relative excess risk due interaction, 9.08 [-0.22 to 43.18]). Synergistic effect followed a dose-dependent pattern with both recent and cumulative SHS exposures, with relative excess risk due interaction for parental asthma and over 100 SHS cigarette-years of 6.17 (0.57-19.16). CONCLUSIONS: This is the first study showing that individuals with asthmatic heredity have a considerably increased risk of adult-onset asthma when exposed to SHS. SHS exposure has dose-dependent synergism with family history of asthma, the joint effect being stronger with higher exposure levels. Avoiding SHS could be an important preventive measure for reducing the risk of adult-onset asthma among those with asthmatic heredity. Asking about family history of asthma is a useful tool for identifying these susceptible individuals in clinical and preventive settings.

Full-length visfatin levels are associated with inflammation in women with polycystic ovary syndrome.

BACKGROUND: Polycystic ovary syndrome (PCOS) is the most common gynaecological endocrinopathy characterized by oligomenorrhea, amenorrhoea, clinical and/or biochemical hyperandrogenism and polycystic ovaries. Abdominal deposition of excess body fat and metabolic diseases like insulin resistance and compensatory hyperinsulinemia are commonly observed in PCOS subjects. It has been suggested that visfatin is an adipokine secreted from the abdominal fat influencing glucose metabolism and might therefore contribute to the metabolic disturbances in PCOS. MATERIALS AND METHODS: We measured circulating full-length visfatin levels with a specific enzyme immunoassay (AdipoGen Inc, Incheon, South-Korea) in 57 women with self-reported symptoms of PCOS (hirsutism and/or oligomenorrhea) and ultrasound confirmed polycystic ovaries, and in 57 controls from the Northern Finland 1966 Birth Cohort and explored its association with metabolic and inflammatory parameters. RESULTS: Polycystic ovary syndrome cases had higher body mass index (BMI) (25·7 vs. 24·1 kg/m(2)) and waist circumference (83·2 vs. 78·8 cm) compared to controls, yet there was no difference in plasma visfatin levels between them. In contrast, visfatin significantly correlated with C-reactive protein (CRP) in the control group and with white blood cell count (WBC) in both groups. In linear regression analysis, adjusted for PCOS, smoking, socioeconomic status, BMI or waist circumference, serum lipids and markers of glucose metabolism and hormone status, only WBC remained significantly associated with plasma visfatin levels. CONCLUSION: Our results suggest that circulating visfatin levels correlate with WBC and CRP but are not associated with PCOS, obesity or metabolic markers, suggesting that visfatin may act as a proinflammatory cytokine.

Association of IL-6 and IL-6R gene polymorphisms with susceptibility to respiratory tract infections in young Finnish men.

Interleukin-1 (IL-6) is an important mediator of inflammatory response in the respiratory tract during an infection, and the action of IL-6 is mediated by an IL-6 receptor. Several polymorphisms in the IL-6 and IL-6R genes have been associated with different inflammatory disease states. We studied the association between 2 IL-6 (IL6A and IL6B) and 5 IL-6R gene polymorphisms (IL6R1 to IL6R5) and respiratory infections in 511 Finnish military recruits whose respiratory infectious episodes were followed during 6 months of service. A promoter polymorphism of the IL-6R gene, IL6R1 (-183G/A), and two intron 1 polymorphisms, IL6R2 (A/G) and IL6R3 (T/A), were associated with infections. The strongest associations were found for the IL6R1 and IL6R2 polymorphisms, which were in the same linkage disequilibrium block. Conscripts with the A/A (IL6R1), G/G (IL6R2), and A/A (IL6R3) genotypes had an increased risk for respiratory infections during service as follows: odds ratio (OR) 1.72, 95% confidence interval (CI) 1.35-2.19; OR 1.66, 95% CI 1.23-2.26; and OR 1.23, 95% CI 0.98-1.55, respectively. IL-6 gene polymorphism IL6A (-174C/G) was associated with infections only in combination with an IL-6R polymorphism. Our data suggest that polymorphisms in the 5' area of the IL-6R gene may be associated with increased susceptibility to respiratory infections.

Low mannose-binding lectin levels and MBL2 gene polymorphisms associate with Chlamydia pneumoniae antibodies.

OBJECTIVE: Mannose-binding lectin (MBL) has been shown to inhibit infection of host cells by Chlamydia pneumoniae in vitro. We studied if MBL levels and MBL2 polymorphisms associate with the presence of C. pneumoniae antibodies in vivo. MATERIALS AND METHODS: Single nucleotide polymorphisms (SNPs) of the MBL2 gene (promoter alleles H/L, X/Y and P/Q; and exon 1 variant alleles B, C and D and wild-type allele A) were genotyped and serum MBL concentrations and C. pneumoniae IgG, IgA and IgM antibodies were analysed in 889 Finnish military recruits. RESULTS: An MBL level below the median concentration and the MBL2 P/P genotype were significant risk factors of IgG or IgA seroconversions or the presence of IgM antibodies during military service (adjusted odds ratio (OR) 1.5; 95% confidence interval (CI) 1.1-2.1 and OR 1.5; 95% CI 1.0-2.2, respectively). In addition, the promoter Y/Y (OR 1.6; 95% CI 1.1-2.3) and exon 1 variant allele genotypes (OR 1.4; 95% CI 1.0-2.0) were possibly associated with elevated antibodies. CONCLUSIONS: These results suggest, for the first time, that low serum MBL levels and MBL2 polymorphisms may associate with elevated C. pneumoniae antibodies and seroconversions and thus support the previous findings in vitro.

Quantification of Chlamydia pneumoniae in cultured human macrophages and HL cells: comparison of real-time PCR, immunofluorescence and ELISA methods.

Chlamydia pneumoniae is an intracellular gram-negative bacterium, which replicates only in eukaryotic cells. Quantification of C. pneumoniae in cell culture is needed when studying e.g. the effect of drugs or host cell factors on infectivity and replication. Conventionally, this has been performed by immunofluorescence staining and microscopic counting of chlamydial inclusions. However, this method is usable only if the cell numbers do not fluctuate in cell culture vials and the inclusions are uniform. In macrophages, inclusions are often aberrant, their sizes vary, and multiple inclusions are also seen. Therefore, methods are needed to quantify exact amounts of C. pneumoniae in cells. Here, we describe a new method based on the real-time PCR quantification of chlamydial genomes adjusted to the number of human genomes in cultures. In human epithelial (HL) cell cultures, the C. pneumoniae inclusion numbers and the ratio of C. pneumonia genomes/human genome (Cpn/Hum) correlated significantly (r = 0.978, p < 0.001); thus with HL cells, both methods are usable. However, in macrophage cultures, the correlation was weaker (r = 0.133, p = 0.036) and we recommend PCR quantification for exact measurements.

New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.

Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes.

Smoking status interacts with the association between mannose-binding lectin serum levels and gene polymorphism and the carriage of oropharyngeal bacteria.

Mannose-binding lectin (MBL) role in the carriage of oropharyngeal bacteria is not known. We investigated the association of smoking, MBL2 polymorphisms, and MBL concentrations with oropharyngeal carriage of respiratory bacteria in young men. Oropharyngeal specimens, MBL concentrations, and MBL2 gene polymorphisms were measured in 124 asthmatic and 394 nonasthmatic Finnish military recruits. The carriage rates of S. pneumoniae (p = 0.002), N. meningitidis (p = 0.005), and beta-hemolytic streptococci (p < 0.001) throughout the military service were significantly higher among smokers than in nonsmokers. An MBL level below the median proved to be a significant risk factor for the carriage of N. meningitidis (odds ratio [OR] = 1.9; 95% confidence interval [CI] 1.0-3.6) and beta-hemolytic streptococci (OR = 2.0; 95% CI 1.2-3.2) in the nonsmokers and a borderline significant risk factor for the carriage of S. pneumoniae (OR = 1.5; 95% CI 0.9-2.6), whereas low MBL levels producing MBL2 haplotypes (LXA/LXA, LXA/O, HYA/O, LYA/O, O/O) seemed to be associated with the carriage of N. meningitidis (OR = 1.8; 95% CI 1.0-3.4) and S. pneumoniae (OR = 1.6; 95% CI 0.9-2.7). Thus, MBL deficiency may predispose nonsmokers to oropharyngeal carriage of these bacteria. We hypothesize that the major factor contributing to elevated bacterial carriage in smokers might be increased bacterial adherence to epithelial cells, which obscures the effect of MBL.