Exposure to ambient nitrogen dioxide (NO₂) has been linked to increased mortality in several epidemiological studies but the question remains of whether NO₂is directly responsible for the health effects or is only an indicator of other pollutants, including particulate matter. The aim of the present review was to provide pooled estimates of the long-term effects of NO₂on mortality, which are potentially useful for health impact assessment.We selected 23 papers, published from 2004 to 2013, evaluating the relationship between NO₂and mortality, also including an assessment of the effect of particulate matter exposure. A random-effects meta-analysis was carried out on 19 studies.The pooled effect on mortality was 1.04 (95% CI 1.02–1.06) with an increase of 10 μg·m⁻³in the annual NO₂concentration and 1.05 (95% CI 1.01–1.09) for particulate matter <2.5 μm in diameter (PM_2.5) (10 μg·m⁻³). The effect on cardiovascular mortality was 1.13 (95% CI 1.09–1.18) for NO₂and 1.20 (95% CI 1.09–1.31) for PM_2.5. The NO₂effect on respiratory mortality was 1.03 (95% CI 1.02–1.03) and 1.05 (95% CI 1.01–1.09) for PM_2.5. Four bipollutant analyses with particulate matter and NO₂in the same models showed minimal changes in the effect estimates of NO₂.There is evidence of a long-term effect of NO₂on mortality as great as that of PM_2.5. An independent effect of NO₂emerged from multipollutant models.

Short-term effects of air pollutants on respiratory mortality and morbidity have been consistently reported but usually studied separately. To more completely assess air pollution effects, we studied hospitalisations for respiratory diseases together with out-of-hospital respiratory deaths.A time-stratified case-crossover study was carried out in six Italian cities from 2001 to 2005. Daily particulate matter (particles with a 50% cut-off aerodynamic diameter of 10 μm (PM₁₀)) and nitrogen dioxide (NO₂) associations with hospitalisations for respiratory diseases (n = 100 690), chronic obstructive pulmonary disease (COPD) (n = 38 577), lower respiratory tract infections (LRTI) among COPD patients (n = 9886) and out-of-hospital respiratory deaths (n = 5490) were estimated for residents aged ≥35 years.For an increase of 10 μg·m⁻³in PM₁₀, we found an immediate 0.59% (lag 0–1 days) increase in hospitalisations for respiratory diseases and a 0.67% increase for COPD; the 1.91% increase in LRTI hospitalisations lasted longer (lag 0–3 days) and the 3.95% increase in respiratory mortality lasted 6 days. Effects of NO₂were stronger and lasted longer (lag 0–5 days). Age, sex and previous ischaemic heart disease acted as effect modifiers for different outcomes.Analysing multiple rather than single respiratory events shows stronger air pollution effects. The temporal relationship between the pollutant increases and hospitalisations or mortality for respiratory diseases differs.

Background: Although damage to the respiratory system from air pollutants has been recognized, research on susceptibility to air pollution in patients with chronic obstructive respiratory disease (COPD) has produced contradictory results. We studied the short-term effects of particulate matter (PM₁₀, PM_2.5), nitrogen dioxide (NO₂), and ozone (O₃) on cardiac and respiratory mortality in a COPD cohort. We assessed age, sex, and previous diseases as effect modifiers. Methods: Using hospital data (1998–2009) and pharmaceutical data (2005–2009), we enrolled 145,681 COPD subjects, aged 35+ years and residents of Rome, and followed them from 2005 to 2009. A comparison group of people without COPD (1,710,557 subjects) was also studied. We analyzed deaths due to all natural causes (International Classification of Diseases - Ninth Revision codes 1–799). Statistical analyses were carried out using Poisson regression and a case-crossover approach. Results: PM₁₀, PM_2.5, and NO₂ (0- to 5-day lag) were associated with daily mortality, with stronger effects in people with COPD. The mortality associated with PM₁₀ (per interquartile range [IQR] = 16 μg/m³) was five times more in COPD patients (3.5% [95% confidence interval = −0.1% to 7.2%]) than in other subjects (0.7% [−0.8% to 2.2%]). Effects on respiratory mortality among COPD subjects were particularly elevated from PM_2.5 (IQR = 11 μg/m³) (11.6% [2.0% to 22.2%]) and NO₂ (IQR = 24 μg/m³) (19.6% [3.5% to 38.2%]). Older age, male sex, preexisting heart conduction disorders, and cerebrovascular diseases were associated with stronger effects in COPD subjects. Conclusions: COPD patients are more susceptible to air pollutants, especially PM₁₀ and NO₂. These results suggest a need for more protective air pollution standards for susceptible groups.

Estimating COPD occurrence is perceived by the scientific community as a matter of increasing interest because of the worldwide diffusion of the disease. We aimed to estimate COPD prevalence by using administrative databases from a city in central Italy for 2002–2006, improving both the sensitivity and the reliability of the estimate. Multiple sources were used, integrating the hospital discharge register (HDR), clinical charts, spirometry and the cause-specific mortality register (CMR) in a longitudinal algorithm, to reduce underestimation of COPD prevalence. Prevalence was also estimated on the basis of COPD cases confirmed through spirometry, to correct misclassification. Estimating such prevalence relied on using coefficients of validation, derived as the positive predictive value (PPV) for being an actual COPD case from clinical and spirometric data at the Institute of Clinical Physiology of the National Research Council. We found that sensitivity of COPD prevalence increased by 37%. The highest estimate (4.43 per 100 residents) was observed in the 5-year period, using a 3-year longitudinal approach and combined data from three sources. We found that 17% of COPD cases were misclassified. The above estimate of COPD prevalence decreased (3.66 per 100 residents) when coefficients of validation were applied. The PPV was 80% for the HDR, 82% for clinical diagnoses and 91% for the CMR. Adjusting the COPD prevalence for both underestimation and misclassification of the cases makes administrative data more reliable for epidemiological purposes.

There is large epidemiological evidence on the short-term health effects of O₃ and NO₂. These gaseous pollutants induce oxidative stress through their oxidative potential. Therefore, the evaluation of their combined oxidative capacity (O_x) has been proposed rather than studying the effect of either gas individually. To study the short-term effects of daily concentrations of O₃, NO₂, and O_x on mortality in Rome, in 2002–2015, daily deaths from the city mortality registry were analyzed along with O₃ and NO₂ levels observed in Rome and with estimated O_x and O_wt (O_x, weighted by the redox potential of O₃ and NO₂). A Poisson regression model was used considering trends, and meteorological and population changes. The effects on mortality were estimated at lag 0–1 and 0–5 for 10 μg/m³. O₃ and NO₂ were associated with mortality, with the highest effects at lag 0–5, 0.81% (0.45–1.17) and 2.72% (2.07–3.37), respectively. O_x had an intermediate effect between the two gases. After adjusting for PM₁₀, O_wt had a stronger effect (1.72%; 1.14–2.30) than either gas, 0.86% (0.50–1.22) for O₃ and 1.61% (1.15–2.06) for NO_2. Both O_x and O_wt were associated with cerebrovascular, respiratory and, to a lesser extent, cardiac mortality more than either gas. These results suggest that the use of O_x (or O_wt) can provide a better assessment of the combined role of O₃ and NO₂ on mortality and can avoid the uncertainty of the threshold level for ozone. The brain and lungs seem to be the main targets of O₃ and NO_2.

Background: Mortality and cardiorespiratory diseases are well-documented effects of atmospheric pollutants. Because epigenetic mechanisms are identified as interaction factors between environmental exposures and gene expression, as well as pathogenic factors of impaired immune tolerance, it seems relevant to study autoimmune diseases in relation to air pollution. Methods: To study whether daily increases of particulate matter (PM₁₀, PM_2.5) and nitrogen dioxide (NO₂) are associated with exacerbations of autoimmune diseases, a total of 23,898 residents of Rome (Italy) who were diagnosed in 2003–2014 with Hashimoto thyroiditis, systemic lupus erythematosus, rheumatoid arthritis, psoriasis, and multiple sclerosis were enrolled. Exacerbations were defined as subsequent hospitalizations for the initial disease or its complications, or a different autoimmune disease, and as dose increases or time reductions between drug prescriptions for autoimmune diseases. Data were analyzed for 2006–2014. Daily concentrations of PM₁₀, PM_2.5, and NO₂ in Rome were available from a fixed monitoring network, during 2006–2014. A time-stratified case-crossover study was carried out. Results: All air pollutants were associated with more frequent changes than usual in treatment for all autoimmune diseases; the greatest increases in risk were observed for PM_2.5 (10 μg/m³ increase) in thyroiditis (3.31% [2.21%, 4.2%]), lupus (3.55% [0.70%, 6.49%]), arthritis (4.93% [2.11%, 7.83%]), and psoriasis (4.04% [0.21%, 8.01%]). No associations were observed for hospitalizations for all studied diseases, whereas changes toward lower corticosteroids’ dose in multiple sclerosis and less effective corticosteroids’ forms in psoriasis were observed. Conclusions: PM_2.5 and NO₂ might exacerbate autoimmune diseases. As detected with treatment changes especially in younger patients.