Pollution's Impact: Skeletal System Under Threat

Air pollution is a critical environmental and health issue in both developing and developed countries. According to the World Health Organization (WHO), around 91% of the world’s population was living with poor air quality in 2016.

Air pollution is associated with inflammation and oxidative stress, which predispose to several chronic diseases in humans, including osteoporosis.

Osteoporosis is a chronic age-related disease of the skeletal system associated with changes in endocrine, metabolic and mechanical factors.

Recent studies have shown that air pollution predisposed the public to a higher risk of osteoporosis.

The negative effects of air pollution are partly attributed to particulate matter (PM). PM can penetrate the lower respiratory tract and has harmful direct and indirect effects on different organs and tissues.

Some of the fixed and modifiable risk factors of osteoporosis include sex (female), old age, ethnicity, low body mass index (BMI), menopause, low physical activity, malnutrition, use of glucocorticoid, smoking, alcohol consumption and chronic diseases like diabetes and chronic kidney disease (CKD).

Air pollution, like smoking, is a modifiable risk factor for osteoporosis.

Air pollution is associated with inflammation and oxidative stress, which can lead to osteoporosis and other chronic diseases

Air pollution is a global health problem, with 9 out of 10 people worldwide breathing polluted air. It is the second most important risk factor associated with noncommunicable diseases after smoking. Air pollution is estimated to have caused 4.2 million premature deaths worldwide in 2016, with 58% of these being due to cardiovascular disease, 18% to respiratory disease, and 6% to lung cancer.

Air pollution is associated with systemic inflammation, which can affect bone metabolism through the specific effect of cytokines such as TNFα, IL-1β, IL-6, and IL-17 on osteoblast and osteoclast differentiation and function.

Some pollutants, particularly certain gas and metal compounds, can cause oxidative damage in the airway and bone cells. Oxidative stress is characterised by the increase in free radicals, which can modify signalling pathways and dysregulate the signalling pathways. Reactive species can also modify the patterns of gene expression by acting on certain transcription factors.

Different groups of pollutants can act as endocrine disruptors when binding to the receptors in bone cells, changing their functioning. Endocrine-disrupting chemicals (EDCs) are exogenous chemical substances that affect hormone activity. Some EDCs are in polluted air as volatile or semi-volatile organic compounds in gaseous form or are bound to particles.

Air pollution can directly and indirectly cause vitamin D deficiency. Ozone is a gas in the stratosphere and troposphere. In the stratosphere, ozone protects against the damaging effects of the sun by absorbing UV radiation, whereas in the troposphere, ozone harms health by acting as an environmental pollutant. Tropospheric ozone production depends on the photochemical interaction of nitrogen oxides and volatile organic compounds. The anthropogenic sources of these compounds are fossil fuel and biomass burning, as well as solvent evaporation.

Knowing the mechanisms of bone damage induced by exposure to air pollution will contribute to improved understanding of the physiopathology of bone damage associated with environmental exposure, as well as to implementing new and better prevention strategies.

Air pollution can cause vitamin D deficiency, which is essential for bone health

Air pollution is a critical environmental and health issue in both developing and developed countries. According to the World Health Organization (WHO), around 91% of the world's population was living with poor air quality in 2016. Air pollution is associated with the incidence of pulmonary and non-pulmonary diseases, including metabolic disorders, cardiovascular diseases, central nervous system diseases, and cancer.

Air pollutants can be categorised into gaseous or solid types. The common examples of gaseous pollutant are ammonia, nitrogen dioxide (NO2), carbon monoxide (CO), sulphur dioxide (SO2), tropospheric or ground-level ozone (O3) and volatile organic compounds. Particulate matter (PM) is the sum of heterogeneous solid air pollutants, comprising water, dust and particles.

Ozone (O3) is a gas in the stratosphere and troposphere. In the stratosphere, ozone protects against the damaging effects of the sun by absorbing UV radiation, whereas in the troposphere, it harms health by acting as an environmental pollutant. Tropospheric ozone production depends on the photochemical interaction of nitrogen oxides (NOx) and volatile organic compounds (VOCs). The anthropogenic sources of NOx and VOCs are fossil fuel and biomass burning, as well as solvent evaporation.

Since it absorbs UV radiation, ozone has been proposed by several studies to be responsible for low UVB exposure and deficient vitamin D synthesis. A cross-sectional study of a cohort of 85 postmenopausal Caucasian women in Belgium who lived in rural and urban areas revealed that women who lived in cities were exposed to three times as much ground-level ozone as those living in rural areas. Likewise, women living in cities showed higher prevalence of having 25-hydroxyvitamin D levels below 75 nmol/L, even though they had a higher solar exposure index (SEI). This could be the result of low UVB exposure from high tropospheric ozone levels. It is well-documented that UV radiation is essential for the skin to synthesize vitamin D, and its deficiency affects calcium absorption, which in turn leads to bone density reduction and increased risk of osteoporosis-related fractures.

Some studies show an association between air pollution and risk of vitamin D deficiency; however, these studies usually combine the values of PM2.5, NO2, and CO. Such studies do not examine the O3 levels separately or do not mention how they measured air pollution levels. Thus, studies are needed in which ozone levels are measured individually along with UVB levels and concentrations of serum vitamin D.

Air pollution can cause endocrine disruption, which can affect bone health

Endocrine disruptors can interfere with the action of hormones at many different steps. They may act by altering hormone synthesis in the endocrine gland, or through altering transport of the hormone to the target organ by interfering with the activity of conjugation enzymes or by competing for binding to carrier proteins. Alternatively, they may act through altering metabolism/excretion of the hormone or through competing with the hormone for binding to a receptor in target cells and in so doing to mimic action of steroid hormones (particularly, but not exclusively, in relation to the action of estrogens and androgens) and thyroid hormones.

Endocrine disruptors are associated with deleterious effects on male and female reproductive health; causes diabetes, obesity, metabolic disorders, thyroid homeostasis and increase the risk of hormone-sensitive cancers.

There is a considerable body of evidence documenting the presence of endocrine disruptors in both outdoor and indoor air, that endocrine disruptors are entering human tissues, and that endocrine disruptors are impacting on human endocrine health. However, the extent to which air-borne endocrine disruptors contribute to the overall human body burdens of endocrine disruptors is unknown, and instances where endocrine abnormalities can be related directly and solely to an airborne source of endocrine disruptors are few.

Air pollution can cause oxidative stress, which can lead to bone damage

Air pollution is a critical environmental and health issue, with 91% of the world's population living with poor air quality. It is associated with inflammation and oxidative stress, which can lead to several chronic diseases in humans.

Oxidative stress is a phenomenon where there is an increase in free radicals, such as reactive oxygen species and reactive nitrogen species. These reactive species can modify signalling pathways and oxidise or reduce redox-sensitive amino acid residues, keeping them active and leading to sustained expression of certain proteins that promote cell proliferation, apoptosis, and inflammatory responses.

Additionally, air pollution can cause low-grade systemic inflammation, which affects bone metabolism through the specific effect of cytokines such as TNFα, IL-1β, IL-6, and IL-17 on osteoblast and osteoclast differentiation and function.

Air pollution can also act as endocrine disruptors when binding to the receptors in bone cells, changing their functioning.

Air pollution can cause low-grade systemic inflammation, which can affect bone metabolism

Additionally, air pollution can cause oxidative damage in the airway and bone cells. Reactive species and their damage to cells can modulate the inflammatory response. Reactive species can oxidise or reduce redox-sensitive amino acid residues, changing the structure or function of some signalling proteins and keeping them active. Consequently, signal transductions stay active and lead to sustained expression of certain proteins that promote cell proliferation, apoptosis, and inflammatory responses.

Air pollution can also act as endocrine disruptors when binding to the receptors in bone cells, changing their functioning. For example, phthalates, which are commonly found in the atmosphere, can affect the nuclear translocation of fibroblast growth factor 2 (FGF2) in osteoblasts, which is essential for osteoblast function and differentiation.

Finally, air pollution can cause vitamin D deficiency. Ozone (O3) is a gas in the stratosphere and troposphere. In the troposphere, ozone harms health by acting as an environmental pollutant. Tropospheric ozone production depends on the photochemical interaction of nitrogen oxides (NOx) and volatile organic compounds (VOCs). The anthropogenic sources of NOx and VOCs are fossil fuel and biomass burning, as well as solvent evaporation. Since it absorbs UV radiation, ozone has been proposed by several studies to be responsible for low UVB exposure and deficient vitamin D synthesis.

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