Background: Low birth weight (LBW) infants do not form a homogeneous group; LBW can be caused by prematurity or poor fetal growth manifesting as small for gestational age (SGA) infants or intrauterine growth retardation. We aimed to clarify the relationship of maternal smoking with both SGA and preterm LBW infants. Methods: The study population comprised pregnant women who registered at the Koshu City between January 1, 1995, and December 31, 2000, and their children. We performed multivariate analyses using multiple logistic regression models to clarify the relationship of maternal smoking during pregnancy with the SGA outcome and preterm birth in LBW infants. Results: In this study period, 1,329 pregnant women responded to questionnaires, and infant data were collected from 1,100 mothers (follow-up rate: 82.8%). The number of LBW infants was 81 (7.4%). In this cohort, maternal smoking during early pregnancy was associated with LBW and the SGA outcome. Maternal smoking during early pregnancy was a risk factor for LBW with SGA outcome and for LBW with full-term birth. However, it was not a risk factor for LBW with appropriate weight for gestational age (AGA) and LBW with preterm birth. Conclusion: These results suggested that LBW with AGA and LBW with preterm birth were associated with other risk factors that were not considered in this study, such as periodontal disease. For the prevention of LBW, not only abstinence from smoking during pregnancy but also other methods such as establishing a clinical setting should be adopted.
Background: The effects of airborne particulate matter (PM) are a major human health concern. In this panel study, we evaluated the acute effects of exposure to PM on peak expiratory flow (PEF) and wheezing in children. Methods: Daily PEF and wheezing were examined in 19 asthmatic children who were hospitalized in a suburban city in Japan for approximately 5 months. The concentrations of PM less than 2.5 μm in diameter (PM2.5) were monitored at a monitoring station proximal to the hospital. Moreover, PM2.5 concentrations inside and outside the hospital were measured using the dust monitor with a laser diode (PM2.5(LD)). The changes in PEF and wheezing associated with PM concentration were analyzed. Results: The changes in PEF in the morning and evening were significantly associated with increases in the average concentration of indoor PM2.5(LD) 24 h prior to measurement (-2.86 L/min [95%CI: -4.12, -1.61] and -3.59 L/min [95%CI: -4.99, -2.20] respectively, for 10-μg/m3 increases). The change in PEF was also significantly associated with outdoor PM2.5(LD) concentrations, but the changes were smaller than those observed for indoor PM2.5(LD). Changes in PEF and concentration of stationary-site PM2.5 were not associated. The prevalence of wheezing in the morning and evening were also significantly associated with indoor PM2.5(LD) concentrations (odds ratios = 1.014 [95%CI: 1.006, 1.023] and 1.025 [95%CI: 1.013, 1.038] respectively, for 10-μg/m3 increases). Wheezing in the evening was significantly associated with outdoor PM2.5(LD) concentration. The effects of indoor and outdoor PM2.5(LD) remained significant even after adjusting for ambient nitrogen dioxide concentrations. Conclusion: Indoor and outdoor PM2.5(LD) concentrations were associated with PEF and wheezing among asthmatic children. Indoor PM2.5(LD) had a more marked effect than outdoor PM2.5(LD) or stationary-site PM2.5.
Background: To show the reduction in life expectancy due to smoking and the recovery of normal life expectancy by smoking cessation is useful for tobacco control health policy. Methods: This study included 140,026 males and 156,810 females aged 40-79 years, who were participants of large-scale cohort studies in Japan (Japan Health Center-based Prospective Study [JPHC]-I, JPHC-II, Three-Prefecture Study, and Japan Collaborative Cohort [JACC] Study), which commenced around 1990. The mean follow-up period (±standard deviation) was 9.6 ± 2.3 years, during which 16,282 men and 9,418 women died. For persons aged 40-79 years grouped according to each defined smoking status in the baseline questionnaire, sex- and age-specific death rates at attained ages were calculated. The age-specific death rate was calculated by dividing the number of persons who died at the age by the number of persons who were followed-up at the attained age. From these death rates, current life tables were constructed according to the smoking status, and survival curves were plotted. Results: The life expectancy of male smokers, ex-smokers, and never-smokers at age 40 years was 38.5, 40.8, and 42.4 years respectively. In women, the corresponding life expectancies were 42.4, 42.1, and 46.1 years. In both sexes, the age by which half of the current smokers had died was approximately 4 years younger than that for never-smokers. The life expectancies of male ex-smokers who quit smoking before ages 40, 50, 60, and 70 years were 4.8, 3.7, 1.6, and 0.5 years longer than those of smokers, respectively. Conclusion: Smoking considerably reduced the life expectancy, and earlier smoking cessation resulted in a better survival than that seen with continued smoking.
Background: Antihypertensive and non-steroidal anti-inflammatory drugs (NSAIDs) are used to treat many common diseases. However, it has been suspected that interactions between these drugs exist. Here, we assessed the interactions between non-selective NSAIDs and several classes of antihypertensive drugs. Methods: The study design was a cohort study using "The Antihypertensive Drug Database," which is a collection of data accumulated from Drug Use Investigations. Subjects newly starting antihypertensive drug therapy were identified in the database. We compared the "User" group, who were co-administered NSAIDs, with the "Non-user" group, who were not. The outcome measure was the change in systolic blood pressure from the baseline after 2 months of treatment. We estimated the non-adjusted and adjusted differences in the change in systolic blood pressure between the "User" and "Non-user" groups. Results: Data were collected for a total of 1,204 subjects, of whom 364 were prescribed beta blockers, 60 were prescribed diuretics, 628 were prescribed angiotensin-converting enzyme inhibitors, and 152 were prescribed calcium channel blockers. The adjusted difference in the change in systolic blood pressure between the User (n = 301) and Non-user (n = 903) groups was 2.88 mmHg (95% confidence interval: 0.89, 4.87); thus, systolic blood pressure in the Non-User group decreased further from the baseline than that in the User group. In subjects administered beta blockers, diuretics, angiotensin-converting enzyme inhibitors, and calcium channel blockers, the corresponding differences were 0.37 mmHg (-3.24, 3.98), 6.11 mmHg (-3.16, 15.37), 3.85 mmHg (1.16, 6.66), and 3.50 mmHg (-2.03, 9.02). Conclusion: The effectiveness of antihypertensive drugs was attenuated by the co-administration of NSAIDs. The differences in the effects of NSAIDs varied with different classes of antihypertensive drugs.
Background: Serum folate concentration is lower in individuals with the methylenetetrahydrofolate reductase (MTHFR) 677TT genotype than in those with the MTHFR 677CC or 677CT genotypes. Since studies considering folate intake are limited, we examined the association between folate intake and serum folate levels, according to the genotype. Methods: The subjects comprised 170 Japanese persons (74 males and 96 females) aged 20-75 years who visited a clinic to test for Helicobacter pylori infection. Folate intake was estimated using a semiquantitative foodfrequency questionnaire, and serum folate was measured in the residual fasting blood samples of the subjects. MTHFR C677T was genotyped using polymerase chain reaction. Results: The geometric means of serum folate level were 6.19, 6.20, and 5.17 ng/mL among the 60 participants with the 677CC genotype, 90 participants with the 677CT genotype, and 20 participants with the 677TT genotype, respectively. No difference was noted in the mean folate intake estimated using the food-frequency questionnaire. Regression analysis showed that loge(serum folate) adjusted for age, sex, and loge(folate intake) was significantly lower among those with the 677TT genotype than among those with the 677CT or 677CC genotypes (p = 0.01). The adjusted reduction in serum folate was 20.2% (95% confidence interval, 5.4-32.6%) in the case of the 677TT genotype relative to the levels in the case of the 677CC/677CT genotypes. When folate intake was adjusted for total energy intake, using the residual method, the slope of the regression line for 677TT was smaller than those of the regression lines for 677CC and 677CT. Conclusion: Individuals with the 677TT genotype may need to consume more folate to maintain serum folate levels similar to those found in individuals with the 677CC/677CT genotypes.
Background: It remains unclear whether serum uric acid level increases after the cessation of smoking. Methods: In 2000, we conducted a cross-sectional study on the effects of smoking cessation on serum uric acid levels by analyzing the results of annual health check-ups in the Japanese male working population (n = 16,642). Results: The serum uric acid level (6.18 mg/dL) was the highest in ex-smokers, followed by that in never-smokers (6.10 mg/dL) and that in current smokers (5.98 mg/dL). Ex-smokers weighed 0.6 kg more than the never-smokers and 1.5 kg more than the current smokers. The frequency of alcohol intake was closely correlated to the smoking habits. The serum uric acid levels declined in all groups, after adjustments for age, body mass index, and alcohol intake, though the levels in ex-smokers were 0.2 mg/dL higher than those in current smokers. Conclusion: The results suggested that alcohol intake contributed considerably to the serum uric acid levels and that smoking itself may have suppressed these levels via metabolic effects or the action of superoxides.
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