Population aging increases the need for knowledge on positive aspects of aging, and contributions of older people to their own wellbeing and that of others. We defined active aging as an individual's striving for elements of wellbeing with activities as per their goals, abilities and opportunities. This study examines associations of health, health behaviors, health literacy and functional abilities, environmental and social support with active aging and wellbeing. We will develop and validate assessment methods for physical activity and physical resilience suitable for research on older people, and examine their associations with active aging and wellbeing. We will examine cohort effects on functional phenotypes underlying active aging and disability.
For this population-based study, we plan to recruit 1000 participants aged 75, 80 or 85 years living in central Finland, by drawing personal details from the population register. Participants are interviewed on active aging, wellbeing, disability, environmental and social support, mobility, health behavior and health literacy. Physical activity and heart rate are monitored for 7 days with wearable sensors. Functional tests include hearing, vision, muscle strength, reaction time, exercise tolerance, mobility, and cognitive performance. Clinical examination by a nurse and physician includes an electrocardiogram, tests of blood pressure, orthostatic regulation, arterial stiffness, and lung function, as well as a review of chronic and acute conditions and prescribed medications. C-reactive protein, small blood count, cholesterol and vitamin D are analyzed from blood samples. Associations of factors potentially underlying active aging and wellbeing will be studied using multivariate methods. Cohort effects will be studied by comparing test results of physical and cognitive functioning with results of a cohort examined in 1989-90.
The current study will renew research on positive gerontology through the novel approach to active aging and by suggesting new biomarkers of resilience and active aging. Therefore, high interdisciplinary impact is expected. This cross-sectional study will not provide knowledge on temporal order of events or causality, but an innovative cross-sectional dataset provides opportunities for emergence of novel creative hypotheses and theories.
Vehicle engine exhaust includes ultrafine particles with a large surface area and containing absorbed polycyclic aromatic hydrocarbons, transition metals and other substances. Ultrafine particles and soluble chemicals can be transported from the airways to other organs, such as the liver, kidneys, and brain. Our aim was to investigate whether air pollution from traffic is associated with risk for other cancers than lung cancer.
We followed up 54,304 participants in the Danish Diet Cancer and Health cohort for 20 selected cancers in the Danish Cancer Registry, from enrolment in 1993-1997 until 2006, and traced their residential addresses from 1971 onwards in the Central Population Registry. We used modeled concentration of nitrogen oxides (NO(x)) and amount of traffic at the residence as indicators of traffic-related air pollution and used Cox models to estimate incidence rate ratios (IRRs) after adjustment for potential confounders.
NO(x) at the residence was significantly associated with risks for cervical cancer (IRR, 2.45; 95% confidence interval [CI], 1.01;5.93, per 100 µg/m(3) NO(x)) and brain cancer (IRR, 2.28; 95% CI, 1.25;4.19, per 100 µg/m(3) NO(x)).
This hypothesis-generating study indicates that traffic-related air pollution might increase the risks for cervical and brain cancer, which should be tested in future studies.
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The influence of temperature on acute myocardial infarction (AMI) has not been investigated as extensively as the effects of broader outcomes of morbidity and mortality. Sixteen studies reported inconsistent results and two considered confounding by air pollution. We addressed some of the methodological limitations of the previous studies in this study.
This is the first study of the association between the daily 3-hour maximum apparent temperature (Tapp(max)) and AMI hospital admissions in Copenhagen. The study period covered 1 January 1999-31 December 2006, stratified in warm (April-September) and cold (October-March) periods. A case-crossover epidemiology study design was applied. Models were adjusted for public holidays and influenza, confounding by PM10, NO2 and CO was investigated, the lag and non-linear effects of Tapp(max) was examined, effect modification by age, sex and SES was explored, and the results of the case-crossover models were compared to those of the generalised additive Poisson time-series and generalised estimating equation models.
14,456 AMI hospital admissions (12,995 people) occurred during the study period. For an inter-quartile range (6 or 7°C) increase in the 5-day cumulative average of Tapp(max), a 4% (95% CI:-2%; 10%) and 9% (95% CI: 3%; 14%) decrease in the AMI admission rate was observed in the warm and cold periods, respectively. The 19-65 year old group, men and highest SES group seemed to be more susceptible in the cold period.
An increase in Tapp(max) is associated with a decrease in AMI admissions during the colder months.
One of the key climate change factors, temperature, has potentially grave implications for human health. We report the first attempt to investigate the association between the daily 3-hour maximum apparent temperature (Tapp(max)) and respiratory (RD), cardiovascular (CVD), and cerebrovascular (CBD) emergency hospital admissions in Copenhagen, controlling for air pollution. The study period covered 1 January 2002-31 December 2006, stratified in warm and cold periods. A case-crossover design was applied. Susceptibility (effect modification) by age, sex, and socio-economic status was investigated. For an IQR (8°C) increase in the 5-day cumulative average of Tapp(max), a 7% (95% CI: 1%, 13%) increase in the RD admission rate was observed in the warm period whereas an inverse association was found with CVD (-8%, 95% CI: -13%, -4%), and none with CBD. There was no association between the 5-day cumulative average of Tapp(max) during the cold period and any of the cause-specific admissions, except in some susceptible groups: a negative association for RD in the oldest age group and a positive association for CVD in men and the second highest SES group. In conclusion, an increase in Tapp(max) is associated with a slight increase in RD and decrease in CVD admissions during the warmer months.
Temperature, a key climate change indicator, is expected to increase substantially in the Northern Hemisphere, with potentially grave implications for human health. This study is the first to investigate the association between the daily 3-hour maximum apparent temperature (Tapp(max)), and respiratory, cardiovascular and cerebrovascular mortality in Copenhagen (1999-2006) using a case-crossover design. Susceptibility was investigated for age, sex, socio-economic status and place of death. For an inter-quartile range (7 °C) increase in Tapp(max), an inverse association was found with cardiovascular mortality (-7% 95% CI -13%; -1%) and none with respiratory and cerebrovascular mortality. In the cold period all associations were inverse, although insignificant.
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Oxidative damage to guanine (8-oxoGua) is one of the most abundant lesions induced by oxidative stress and documented mutagenic. 8-Oxoguanine DNA glycosylase 1 (OGG1) removes 8-oxoGua from DNA by excision. The urinary excretion of 8-oxoGua is a biomarker of exposure, reflecting the rate of damage in the steady state. The aim of this study was to investigate urinary 8-oxoGua as a risk factor for lung cancer. In a nested case-cohort design we examined associations between urinary excretion of 8-oxoGua and risk of lung cancer as well as potential interaction with the OGG1 Ser326Cys polymorphism in a population-based cohort of 25,717 men and 27,972 women aged 50-64 years with 3-7 years follow-up. We included 260 cases with lung cancer and a subcohort of 263 individuals matched on sex, age, and smoking duration for comparison. Urine collected at entry was analysed for 8-oxoGua by HPLC with electrochemical detection. There was no significant effect of smoking or OGG1 genotype on the excretion of 8-oxoGua. Overall the incidence rate ratio (IRR) (95% confidence interval) of lung cancer was 1.06 (0.97-1.15) per doubling of 8-oxoGua excretion. The association between lung cancer risk and 8-oxoGua excretion was significant among men [IRR: 1.17 (1.03-1.31)], never-smokers [IRR: 9.94 (1.04-94.7)], and former smokers [IRR: 1.19 (1.07-1.33)]. There was no significant interaction with the OGG1 genotype, although the IRR was 1.14 (0.98-1.34) among subjects homozygous for Cys326. The association between urinary 8-oxoGua excretion and lung cancer risk among former and never-smokers suggests that oxidative stress with damage to DNA is important in this group.
To profile participants based on reported outdoor physical activity barriers using a data-driven approach, describe the profiles and study their association with unmet physical activity need.
Cross-sectional analyses of 848 community-dwelling men and women aged 75-90 living in Central Finland in 2012. Barriers to outdoor physical activity and unmet physical activity need were enquired with a questionnaire. The latent profiles were identified by profiling participants into latent groups using a mixture modeling technique on the multivariate set of indicators of outdoor physical activity barriers. A path model was used to study the associations of the profiles with unmet physical activity need.
Five barrier profiles were identified. Profile A was characterized with minor barriers, profile B with weather barriers, profile C with health and weather barriers, profile D with barriers concerning insecurity, health and weather; and profile E with mobility and health barriers. The participants in the profiles differed in the proportion of individual and environmental barriers. The risk for unmet physical activity need was highest among people whose severe mobility difficulties restricted their outdoor physical activity.
Outdoor physical activity barriers reflect the imbalance in person-environment fit among older people, manifested as unmet physical activity need.
In older adults, mobility limitations often coexist with overweight or obesity, suggesting that similar factors may underlie both traits. This study examined the extent to which genetic and environmental influences explain the association between adiposity and mobility in older women. Body fat percentage (bioimpedance test), walking speed over 10 m, and distance walked in a 6-min test were evaluated in 92 monozygotic (MZ) and 104 dizygotic (DZ) pairs of twin sisters reared together, aged 63-76 years. Genetic and environmental influences on each trait were estimated using age-adjusted multivariate genetic modeling. The analyses showed that the means (and s.d.) for body fat percentage, walking speed, and walking endurance were 33.2+/-7.3%, 1.7+/-0.3 m/s and 529.7+/-75.4 m, respectively. The phenotypic correlation between adiposity and walking speed was -0.32 and between adiposity and endurance it was -0.33. Genetic influences explained 80% of the association between adiposity and speed, and 65% of adiposity and walking endurance. Cross-trait genetic influences accounted for 12% of the variability in adiposity, 56% in walking speed, and 34% in endurance. Trait-specific genetic influences were also detected for adiposity (54%) and walking endurance (13%), but not speed. In conclusion, among community-living older women, an inverse association was found between adiposity and mobility that was mostly due to the effect of shared genes. This result suggests that the identification of genetic variants for body fat metabolism may also provide understanding of the development of mobility limitations in older women.
Short-term exposure to air pollution has been associated with exacerbation of chronic obstructive pulmonary disease (COPD), whereas the role of long-term exposures on the development of COPD is not yet fully understood.
We assessed the effect of exposure to traffic-related air pollution over 35 years on the incidence of COPD in a prospective cohort study.
We followed 57,053 participants in the Danish Diet, Cancer, and Health cohort in the Hospital Discharge Register for their first hospital admission for COPD between 1993 and 2006. We estimated the annual mean levels of nitrogen dioxide (NO2) and nitrogen oxides (NO(x)) at all residential addresses of the cohort participants since 1971 to an event or 2006 and used indicators of traffic near the residential address at recruitment. We assessed the association between exposure to air pollution and COPD incidence by Cox regression analyses for the full cohort, and for participants with and without comorbid conditions, including asthma, diabetes, or cardiovascular disease.
A first hospital admission for COPD was recorded for 1,786 (3.4%) of 52,799 eligible subjects between recruitment (1993-1997) and 2006. COPD incidence was associated with the 35-year mean NO2 level (hazard ratio, 1.08; 95% confidence interval, 1.02-1.14, per interquartile range of 5.8 µg/m³), with stronger associations in subjects with diabetes (1.29; 1.05-1.50) and asthma (1.19; 1.03-1.38).
Long-term exposure to traffic-related air pollution may contribute to the development of COPD with possibly enhanced susceptibility in people with diabetes and asthma.
The aim of this study was to analyze whether the associations between perceived environmental and individual characteristics and perceived walking limitations in older people differ between those with intact and those with poorer lower extremity performance.
Persons aged 75 to 90 ( N = 834) participated in interviews and performance tests in their homes. Standard questionnaires were used to obtain walking difficulties; environmental barriers to and, facilitators of, mobility; and perceived individual hindrances to outdoor mobility. Lower extremity performance was tested using Short Physical Performance Battery (SPPB).
Among those with poorer lower extremity performance, the likelihood for advanced walking limitations was, in particular, related to perceived poor safety in the environment, and among those with intact performance to perceived social issues, such as lack of company, as well as to long distances.
The environmental correlates of walking limitations seem to depend on the level of lower extremity performance.
Environmental barriers are associated with disability-related outcomes in older people but little is known of the effect of environmental barriers on mortality. The aim of this study was to examine whether objectively measured barriers in the outdoor, entrance and indoor environments are associated with mortality among community-dwelling 80- to 89-year-old single-living people.
This longitudinal study is based on a sample of 397 people who were single-living in ordinary housing in Sweden. Participants were interviewed during 2002-2003, and 393 were followed up for mortality until May 15, 2012.Environmental barriers and functional limitations were assessed with the Housing Enabler instrument, which is intended for objective assessments of Person-Environment (P-E) fit problems in housing and the immediate outdoor environment. Mortality data were gathered from the public national register. Cox regression models were used for the analyses.
A total of 264 (67%) participants died during follow-up. Functional limitations increased mortality risk. Among the specific environmental barriers that generate the most P-E fit problems, lack of handrails in stairs at entrances was associated with the highest mortality risk (adjusted RR 1.55, 95% CI 1.14-2.10), whereas the total number of environmental barriers at entrances and outdoors was not associated with mortality. A higher number of environmental barriers indoors showed a slight protective effect against mortality even after adjustment for functional limitations (RR 0.98, 95% CI 0.96-1.00).
Specific environmental problems may increase mortality risk among very-old single-living people. However, the association may be confounded by individuals' health status which is difficult to fully control for. Further studies are called for.
Exposure to particles in the fine and ultrafine size range has been linked to induction of low-grade systemic inflammation, oxidative stress and development of cardiovascular diseases. Declining levels of endothelial progenitor cells within systemic circulation have likewise been linked to progression of cardiovascular diseases. The objective was to determine if exposure to fine and ultrafine particles from indoor and outdoor sources, assessed by personal and residential indoor monitoring, is associated with altered levels of endothelial progenitor cells, and whether such effects are related to leukocyte-mediated oxidative stress. The study utilized a cross sectional design performed in 58 study participants from a larger cohort. Levels of circulating endothelial progenitor cells, defined as either late (CD34(+)KDR(+) cells) or early (CD34(+)CD133(+)KDR(+) cells) subsets were measured using polychromatic flow cytometry. We additionally measured production of reactive oxygen species in leukocyte subsets (lymphocytes, monocytes and granulocytes) by flow cytometry using intracellular 2',7'-dichlorofluoroscein. The measurements encompassed both basal levels of reactive oxygen species production and capacity for reactive oxygen species production for each leukocyte subset. We found that the late endothelial progenitor subset was negatively associated with levels of ultrafine particles measured within the participant residences and with reactive oxygen species production capacity in lymphocytes. Additionally, the early endothelial progenitor cell levels were positively associated with a personalised measure of ultrafine particle exposure and negatively associated with both basal and capacity for reactive oxygen species production in lymphocytes and granulocytes, respectively. Our results indicate that exposure to fine and ultrafine particles derived from indoor sources may have adverse effects on human vascular health.
To study which individual characteristics and environmental factors correlate with fear of moving outdoors and whether fear of moving outdoors predicts development of mobility limitation.
Observational prospective cohort study and cross-sectional analyses.
Community and research center.
Seven hundred twenty-seven community-living people aged 75 to 81 were interviewed at baseline, of whom 314 took part in a 3.5-year follow-up.
Fear of moving outdoors and its potential individual and environmental correlates were assessed at baseline. Perceived difficulties in walking 0.5 km and 2 km were assessed twice a year over a 3.5-year period.
At baseline, 65% of the women and 29% of the men reported fear of moving outdoors. Poor socioeconomic status; musculoskeletal diseases; slow walking speed; and the presence of poor street conditions, hills in the nearby environment, and noisy traffic correlated with fear of moving outdoors. At the first 6-month follow-up, participants with fear of moving outdoors had more than four times the adjusted risk (odds ratio (OR)=4.6, 95% confidence interval (CI)=1.92-11.00) of developing difficulties in walking 0.5 km and a three times greater adjusted risk (OR=3.10, 95% CI=1.49-6.46) for developing difficulty in walking 2 km compared with those without fear. The difference in the prevalence of walking difficulties remained statistically significant over the 3.5-year follow-up (P=.02 and P=.009, respectively).
Fear of moving outdoors is common in older adults and increases the risk of developing self-reported difficulties in walking 0.5 km and 2 km. Knowledge about individual and environmental factors underlying fear of moving outdoors and finding ways to alleviate fear of moving outdoors are important for community planning and prevention of disability.
The aim of the present study was to examine the contribution of genetic and environmental factors to depressive symptoms among older women. The participants were 102 monozygotic and 115 dizygotic female twin pairs aged 64 to 76 years. Depressive symptoms were assessed by the Center for the Epidemiologic Studies Depression Scale. The contribution of genetic and environmental effects was estimated for the constructed depressiveness factor and for the subscales which were depressed mood, psychomotor retardation, lack of wellbeing and interpersonal difficulties. Of the variance in depressiveness, shared environmental influences accounted for 39% and nonshared environmental influences 61%. For the subscales, 24% to 62% of the variance was explained by individual, and 13% to 23% by shared, environmental factors. Lack of wellbeing had its own moderate additive genetic effect explaining 30% of the variance. This study showed that in older women predominantly environmental factors underlay individual differences in depressiveness; however, the factors varied to some extent between dimensions measured by the subscales.
The purpose of the present study was to examine the relative contribution of genetic and environmental effects on the air-conducted hearing threshold levels at low (0.125-0.5 kHz), mid (1-2 kHz), and high (4-8 kHz) frequencies separately for the better and worse hearing ear in older women. We also examined the distribution of audiogram configurations. Data was analysed using quantitative genetic modelling. As part of the Finnish twin study on aging (FITSA), hearing was measured in 103 monozygotic and 114 dizygotic female twin pairs aged 63-76 years. Approximately every third subject had a flat type, and two-thirds a descending type of audiogram configuration. No significant difference was observed in the distribution of audiogram configurations between zygosity groups. In the better ear, additive genetic effects accounted for 64%-74% of the total variance at different frequencies. For the worse ear, environmental effects were larger. Although overall heritability is rather constant across the frequency spectrum, it is noteworthy that at low and high frequencies frequency-specific genetic and environmental effects together accounted for the majority of the total variance.
Previous studies in young and middle-aged men and women have shown that resting electrocardiographic (ECG) variables are influenced by genetic factors. However, the extent to which resting ECG variables are influenced by genetic factors in older women is unknown. Thus, the aim of this study was to estimate the relative contribution of genetic and environmental influences to individual differences in resting ECG variables among older female twins without overt cardiac diseases.
Resting ECG recordings were obtained from 186 monozygotic and 203 dizygotic twin individuals, aged 63-76 years. Quantitative genetic modeling was used to decompose the phenotypic variance in each resting ECG variable into additive genetic, dominance genetic, shared environmental, and unique environmental influences.
The results showed that individual differences in the majority of the resting ECG variables were moderately to highly explained by additive genetic influences, ranging from 32% for T axis to 72% for TV(5). The results also suggested dominance genetic influences on QRS duration, TV(1), and Sokolow-Lyon voltage (36%, 53%, and 57%, respectively). Unique environmental influences were important for each resting ECG variable, whereas shared environmental influences were detected only for QT interval and QTc.
In older women without overt cardiac diseases, genetic influences explain a moderate to high proportion of individual differences in the majority of the resting ECG variables. Genetic influences are especially strong for T-wave amplitudes, left ventricular mass, and hypertrophy indices, whereas other variables, including heart rate, intervals, and axes, are more affected by environmental influences.
To examine the genetic and environmental sources of variation in self-rated health (SRH) in older female twins and to explore the roles of morbidity, functional limitation, and psychological well-being as mediators of genetic and environmental effects on SRH.
Cross-sectional analysis of twin data.
One hundred two monozygotic and 115 dizygotic female twin pairs aged 63 to 76.
SRH was categorized as good, average, or poor. Morbidity was described using a physician-assessed disease-severity scale together with information about the presence of diabetes mellitus and cancer. Maximal walking speed measured over 10 m was used to assess physical functional limitation; the Mini-Mental State Examination and the Center for Epidemiologic Studies Depression Scale were used to characterize psychological well-being. The contributions of genetic and environmental (defined as familial (shared by siblings) or nonshared (unique to each sibling)) effects were assessed using univariate and multivariate structural equation modeling of twin data.
SRH did not have its own specific genetic effect but shared a genetic component in common with the genetic components underlying liability to disease severity, maximal walking speed, and depressive symptoms. It accounted for 64% of the variation in SRH, with environmental effects accounting for the remaining variation.
The current results suggest that there are no specific genetic effects on SRH but rather that genetic influences on SRH are mediated through genetic influences affecting chronic diseases, functional limitation, and mood.
The purpose of the present study was to examine, first, whether hearing acuity predicts falls and whether the potential association is explained by postural balance and, second, to examine whether shared genetic or environmental effects underlie these associations.
Hearing was measured using a clinical audiometer as a part of the Finnish Twin Study on Aging in 103 monozygotic and 114 dizygotic female twin pairs aged 63-76 years. Postural balance was indicated as a center of pressure (COP) movement in semi-tandem stance, and participants filled in a fall-calendar daily for an average of 345 days after the baseline.
Mean hearing acuity (better ear hearing threshold level at 0.5-4 kHz) was 21 dB (standard deviation [SD] 12). Means of the COP velocity moment for the best to the poorest hearing quartiles increased linearly from 40.7 mm(2)/s (SD 24.4) to 52.8 mm(2)/s (SD 32.0) (p value for the trend = .003). Altogether 199 participants reported 437 falls. Age-adjusted incidence rate ratios (IRRs) for falls, with the best hearing quartile as a reference, were 1.2 (95% confidence interval [CI] = 0.4-3.8) in the second, 4.1 (95% CI = 1.1-15.6) in the third, and 3.4 (95% CI = 1.0-11.4) in the poorest hearing quartiles. Adjustment for COP velocity moment decreased IRRs markedly. Twin analyses showed that the association between hearing acuity and postural balance was not explained by genetic factors in common for these traits.
People with poor hearing acuity have a higher risk for falls, which is partially explained by their poorer postural control. Auditory information about environment may be important for safe mobility.
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A crucial issue for the sustainability of societies is how to maintain health and functioning in older people. With increasing age, losses in vision, hearing, balance, mobility and cognitive capacity render older people particularly exposed to environmental barriers. A central building block of human functioning is walking. Walking difficulties may start to develop in midlife and become increasingly prevalent with age. Life-space mobility reflects actual mobility performance by taking into account the balance between older adults internal physiologic capacity and the external challenges they encounter in daily life. The aim of the Life-Space Mobility in Old Age (LISPE) project is to examine how home and neighborhood characteristics influence people's health, functioning, disability, quality of life and life-space mobility in the context of aging. In addition, examine whether a person's health and function influence life-space mobility.
This paper describes the study protocol of the LISPE project, which is a 2-year prospective cohort study of community-dwelling older people aged 75 to 90 (n?=?848). The data consists of a baseline survey including face-to-face interviews, objective observation of the home environment and a physical performance test in the participant's home. All the baseline participants will be interviewed over the phone one and two years after baseline to collect data on life-space mobility, disability and participation restriction. Additional home interviews and environmental evaluations will be conducted for those who relocate during the study period. Data on mortality and health service use will be collected from national registers. In a substudy on walking activity and life space, 358 participants kept a 7-day diary and, in addition, 176 participants also wore an accelerometer.
Our study, which includes extensive data collection with a large sample, provides a unique opportunity to study topics of importance for aging societies. A novel approach is employed which enables us to study the interactions of environmental features and individual characteristics underlying the life-space of older people. Potentially, the results of this study will contribute to improvements in strategies to postpone or prevent progression to disability and loss of independence.
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To explore associations of exposure to ambient and indoor air particulate and bio-aerosol pollutants with cardiovascular and respiratory disease markers, we utilized seven repeated measurements from 48 elderly subjects participating in a 4-week home air filtration study. Microvascular function (MVF), lung function, blood leukocyte counts, monocyte adhesion molecule expression, C-reactive protein, Clara cell protein (CC16) and surfactant protein-D (SPD) were examined in relation to exposure preceding each measurement. Exposure assessment included 48-h urban background monitoring of PM10, PM2.5 and particle number concentration (PNC), weekly measurements of PM2.5 in living- and bedroom, 24-h measurements of indoor PNC three times, and bio-aerosol components in settled dust on a 2-week basis. Statistically significant inverse associations included: MVF with outdoor PNC; granulocyte counts with PM2.5; CD31 expression with dust fungi; SPD with dust endotoxin. Significant positive associations included: MVF with dust bacteria; monocyte expression of CD11 with PM2.5 in the bedroom and dust bacteria and endotoxin, CD31 expression with dust serine protease; serum CC16 with dust NAGase. Multiple comparisons demand cautious interpretation of results, which suggest that outdoor PNC have adverse effects on MVF, and outdoor and indoor PM2.5 and bio-aerosols are associated with markers of inflammation and lung cell integrity.
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