Bronchial Asthma: Prevention

To prevent bronchial asthma, attention must be paid to reducing individual risk factors. Behavioral risk factors

• Diet
  • High intake of fat, sugar, and salt; high prevalence (disease incidence) of severe bronchial asthma
  • Micronutrient deficiency (vital substances) – see prevention with micronutrients.
• Consumption of stimulants
  • Tobacco (smoking)
    • A link between smoking and asthma can be demonstrated in more than 70 percent of asthma patients! Children of smoking parents also have a greatly increased risk of asthma.
    • Maternal smoking (at least 5 cigarettes per day) throughout pregnancy is associated with an increased risk of early and persistent wheezing (OR 1.24) and bronchial asthma (OR 1.65) for the child.
• Physical activity
  • Physical exertion – If an asthma attack occurs about five minutes after the completion of physical exertion or during exertion, it is called exertion-induced asthma.
• Psycho-social situation
  • Stress – it is undisputed that emotional factors significantly influence the course of the disease.
• Overweight (BMI ≥ 25; obesity).
  • Overweight individuals have a threefold higher risk of developing bronchial asthma. Obesity can activate a gene in the lungs that can control inflammation in the lungs.
  • Children with consistently high BMI into school age were most often diagnosed with bronchial asthma:
    • Age and sex adjusted odds ratio (aOR): 2.9.
    • Allergic asthma aOR: 4.7
  • Obesity increased the risk of asthma by 26% (RR 1.26; 1.18-1.34). Obese children developed bronchial asthma confirmed by spirometry (lung function testing) in 29% (RR: 1.29; 1.16-1.42).

Medications

• Antidepressants – the use of older antidepressants in pregnancy was associated with an increased risk of asthma
• Asthma can also be triggered by the use of analgesics (painkillers) – analgesic-induced bronchial asthma (analgesic asthma). These include, for example, acetylsalicylic acid (ASA; aspirin exacerbated respiratory disease, AERD) and nonsteroidal anti-inflammatory drugs (NSAID; NSAID-exacerbated respiratory disease, NERD), which interfere with prostaglandin metabolism. This is a genetically determined pseudoallergic reaction.
• The Norwegian Mother and Child Cohort Study was able to demonstrate with regard to paracetamol exposure that in:
  • Paracetamol intake before pregnancy, there was no association with the risk of asthma in the child.
  • Prenatal exposure, the adjusted asthma rate was 13% higher in three-year-olds and 27% higher in seven-year-olds than in unexposed children.
  • Exclusive exposure during the first six months of life, the adjusted asthma rate was 29% higher in three-year-olds and 24% higher in seven-year-olds.
• A British-Swedish research team considers that the association between the use of certain analgesics during pregnancy and a predisposition of the child to asthma is proven, but not causal. According to these authors, the association can probably be attributed to maternal influences such as anxiety, stress or chronic pain.
• Paracetamol/acetaminophen (children who received paracetamol in the first years of life are more likely to develop bronchial asthma and allergic rhinitis (hay fever) later).
• Beta blockers also often trigger asthma attacks!
• H2-receptor antagonists/proton pump inhibitors (proton pump inhibitors, PPI; acid blockers) – taken during pregnancy for heartburn increases children’s risk by 40% (H2-receptor antagonists) or 30% (proton pump inhibitors) of developing bronchial asthma in the first years of life. Note: Pantoprazole and rabeprazole are contraindicated in pregnancy, and omeprazole should be used only after careful risk-benefit consideration, according to the guidelines.

Environmental exposure – intoxications (poisonings).

• Allergens in allergic bronchial asthma. These include:
  • Pollen
  • House dust mite droppings
  • Animal allergens (house dust mite feces, animal dander, feathers): most common causes of perennial allergic asthma are house dust mite allergy and animal dander allergy
  • Feathers
  • Mold spores
  • Food allergens
  • Insect allergens
• Occupational exposureIn some occupational groups, asthma is clustered due to frequent contact with allergenic, irritant, or toxic (poisonous) substances. These are, for example, metal salts – platinum, chromium, nickel -, wood and plant dusts, industrial chemicals. Also known is the so-called baker’s asthma, fungal asthma and also people who work with isocyanates often suffer from asthma.
• Air pollutants: staying in an air and polluted environment (exhaust fumes, particulate matter, nitrous gases, smog, ozone, tobacco smoke).
  • Hazard ratio of 1.05 (1.03 to 1.07) for each 5 µg/m3 increase in particulate matter (PM2.5) concentration and 1.04 (1.03 to 1.04) for a corresponding increase in PM10 concentration.
• Damp walls (mold; during the first year of life).
• Phthalates (mainly as plasticizers for soft PVC) – could lead to permanent epigenetic changes in the genome of the child, which later promote the development of allergic asthma.Note: Phthalates belong to the endocrine disruptors (synonym: xenohormones), which even in the smallest amounts can damage health by altering the hormonal system.
• Cold air and fog
• Repeated exposure to the triggering allergens (e.g., chlorinated water in swimming pools) – e.g., baby swimmingChlorinated water in swimming pools increases the risk of allergic rhinitis (hay fever; allergic rhinitis) and, if predisposed, may increase the frequency of attacks of bronchial asthma. The reason for this is probably that chlorine compounds damage the barrier of the lung epithelium and thus facilitate the penetration of allergens. Since 1980, the water in swimming pools may contain a maximum of 0.3 to 0.6 mg / l free and 0.2 mg / l combined chlorine at a pH between 6.5 and 7.6 according to DIN standards.
• Household sprays – clear dose-response relationship: in individuals who used household sprays at least once a week, the risk of asthma was half that of participants who refrained from doing so; four times a week use of household sprays already led to a doubling of the risk of asthma!
• Cleaning products in the first years of life, especially if they contained fragrances: more often asthma-like respiratory symptoms (“wheezing”) and more often was diagnosed with asthma disease (versus households with a sparing use).

Prevention factors (protective factors)

• Genetic factors:
  • Genetic risk reduction depending on gene polymorphisms:
    • Genes/SNPs (single nucleotide polymorphism; English : single nucleotide polymorphism):
      • Genes: CHI3L1, GSDMB.
      • SNP: rs7216389 in the gene GSDMB
        • Allele constellation: CC (0.69-fold).
      • SNP: rs4950928 in the gene CHI3L1
        • Allele constellation: CG (0.52-fold).
        • Allele constellation: GG (0.52-fold)
• Maternal diet during pregnancy and lactation should be balanced and nutritious.On the consumption patterns of the mother and the effects on the child:
  • however, there is no evidence that dietary restriction (avoidance of potent food allergens) is useful; the opposite seems to be true:
    • Increased maternal consumption of peanuts in the first trimester (first three months of pregnancy) was associated with a 47% lower likelihood of allergic reactions to peanuts.
    • Increased consumption of milk by the mother in the first trimester was associated with less bronchial asthma and less allergic rhinitis.
    • Increased consumption of wheat by the mother in the second trimester was associated with less atopic eczema (neurodermatitis).
  • There is evidence that fish (omega-3 fatty acids; EPA and DHA) in the mother’s diet during pregnancy or lactation is a protective factor for the development of atopic disease in the child.
• Breastfeeding (full breastfeeding) for at least 4 months.
• Breast-milk substitutes in high-risk infants: if the mother cannot breastfeed or cannot breastfeed adequately, the administration of hydrolyzed infant formula is recommended for high-risk infants up to 4 months of age; there is no evidence of a preventive effect for soy-based infant formula; there are no recommendations for goat, sheep, or mare’s milk
• Supplemental feeding from the beginning of 5 months of age is reported to be associated with promoted tolerance development; early fish consumption is reported to have protective value.
• Diet after the 1st year of life: there are no recommendations for allergy prevention in terms of a special diet.
• Food consumption in childhood
  • Increased consumption of foods containing cow’s milk, breast milk, and oats was inversely (unreversely) related to the risk of allergic asthma.
  • Early fish consumption was associated with a lower risk of allergic and nonallergic asthma.
• Exposure to tobacco smoke: tobacco smoke should be avoided – this is especially true during pregnancy.
• Note on vaccinations: there is no evidence that vaccinations increase the risk of allergy; children should be vaccinated according to STIKO recommendations.
• To reduce inhalation of allergens and contact with allergens from pets; furthermore, avoid indoor and outdoor air pollutants, including exposure to tobacco smoke; it is recommended not to acquire a cat in children at risk.
• Body weight: an increased BMI (body mass index) is positively correlated with bronchial asthma – especially in bronchial asthma.

Recommendation!Taking a dietary supplement during pregnancy with omega-3 fatty acids and magnesium, calcium, folic acid and iodine, as well as a dietary supplement with probiotic cultures.

Tertiary Prevention

Tertiary prevention is concerned with preventing the progression or onset of complications in an already manifest disease. The following measures are effective for this purpose:

• Intake of vegetables, fruits and fish.
• Secondhand smoke leads to an increased rate of exacerbations (worsening of the clinical picture) requiring hospitalization in children with asthma. In the center analysis of 25 studies, 450 children were observed over 7, 6 years.