Polycyclic Aromatic Hydrocarbons Induced by Smoking and Air Pollution: Correlation with Oxidative Stress in Chronic Obstructive Pulmonary Disease Patients

Abstract

Oxidative stress is induced by tobacco smoking and is also associated with exposure to air pollution, which are two of the most important risk factors for chronic obstructive pulmonary disease (COPD). The aim of this study was to correlate tobacco use and exposure to air pollution with oxidative stress markers useful in clinical practice in patients with COPD. A total of 102 patients were included and the levels of polycyclic aromatic hydrocarbons (PAHs), malondialdehyde, uric acid and number of packs-years (PY) were determined. Also, six different ratios were used to assess the source of exposure. The results obtained in this study show an admission of pollutants according to smoking status (former smokers/smoker/non-smokers) quantified in average total concentrations for the group of patients with COPD of 4.12 ng/mL, 6.76 ng/mL, 6.04 ng/mL. The six ratios used show that in COPD, the content of PAHs in the blood could be a result of diesel emissions and fuel combustion. Uric acid levels were lower in the smoker group of COPD patients (mean = 5.21 mg/dL), which indicates that oxidative stress is intensified with each cigarette smoked. Additionally, high concentrations of malondialdehyde were quantified for smoking patients diagnosed with COPD (mean = 2.72 µmol/L) compared to former smokers (mean = 2.43 µmol/L) and non-smoking (mean = 2.32 µmol/L) patients, which is another indicator of the implication of smoking in oxidative stress in COPD patients.

HPLC Analysis and Risk Assessment of 15 Priority PAHs in Human Blood Serum of COPD Patient from Urban and Rural Areas, Iasi (Romania)

“…PAHs in biological tissues as human plasma are present because of the important sources of provenience as smoking and occupational exposure [ 25 ]. These compounds are partially metabolized, and the presence in these biological media is not affected by protein binding [ 26 ]. Therefore, the compounds are present in free form, so the determination from these samples is possible as in other types of samples by using solid–liquid extraction using deproteinization, solid-phase extraction, or liquid–liquid extraction [ 27 ].…”

“…PAHs in biological tissues as human plasma are present because of the important sources of provenience as smoking and occupational exposure [25]. These compounds are partially metabolized, and the presence in these biological media is not affected by protein binding [26]. Therefore, the compounds are Second step was wavelength selection of excitation and emission wavelength in order to improve method sensitivity.…”

Role of Endothelial Dysfunction in Development of Chronic Obstructive Pulmonary Conditions

“…Дополняя и усиливая свободнорадикальное и перекисное окисление, упомянутый патологический каскад является связующей нитью в развитии системной сосудистой дисфункции. В специальной литературе активно обсуждается вопрос о связи процессов ремоделирования сосудов малого диаметра в ответ на воздействие табачного дыма с механизмами избыточного фибро-(ОС) [23]. Ткань легких в большом количестве содержит субстрат перекисного окисления липидов -ненасыщенные жирные кислоты, продукты окисления которых стимулируют активность протеинкиназы-С, высвобождение кальция, снижают синтез оксида азота (NO), нарушают эндотелий-зависимую вазодилатацию, дезориентирует механизмы репликации эндотелиальных клеток и ангиогенеза, индуцируют апоптоз.…”

“…Для изучения особенностей системного и регионального кровотока в ответ на воздействия продуктов никотина в зависимости от средств его доставки были обследованы 45 курящих пациентов без АГ и сердечно-сосудистых заболеваний (22 женщины, 23 мужчины; средний возраст -25 (23)(24)(25)(26)(27)(28)(29) определены достоверные различия количества пациентов с ограничением констрикторной (р = 0,020) и дилататорной (р < 0,001) функций до и после курения, независимо от способа доставки никотина. Так, нарушение констрикторной функции СМА до курения было выявлено у 32 лиц (71%), а после курения -у 41 человека (91%).…”

Food-Borne Polycyclic Aromatic Hydrocarbons and Circadian Disruption

“…It was previously reported that up to 60% of lung cancers were caused by B[ a ]P and other PAHs found in cigarettes, with each cigarette potentially containing 20–40 ng of B[ a ]P. The carcinogenic response could also occur in the bladder, breast, cervix, and prostate . According to a recent clinical study investigating the correlation between smoking and oxidative stress in chronic obstructive pulmonary disease patients, B[ a ]P was the most abundant carcinogenic PAH in smokers and was positively correlated with higher serum uric acid levels . Although lower molecular weight PAHs are predominant in commercial cigarettes, B[ a ]P is used as a representative marker for total PAHs based on the strong positive correlation between them .…”