▶️ Answer/Explanation
(a)
- Tobacco smoke contains carcinogens that damage lung tissue and DNA.
- This is the most common cause of lung cancer.
(b)
- Increased cell density in tumour tissue
- Tumour tissue contains more cells per unit area, so more nuclei are visible.
- Reduced or absent air spaces (alveoli)
- In normal lung tissue, large open spaces (alveoli) are present to allow gas exchange.
- In tumour tissue, these air spaces are compressed or replaced by densely packed cells.
- Disorganized tissue structure
- Normal lung tissue has an organized architecture, while tumour tissue appears irregular.
(c)
- Prediction: More cells undergoing mitosis would be visible
- Cells in different mitotic phases (prophase, metaphase, anaphase, telophase) would be present.
- Reason: Rapidly growing tumours have a high mitotic index
- A higher mitotic index indicates increased cell division.
- This is due to loss of normal cell cycle control in cancer cells.
Markscheme:
(a) Causes of lung cancer:
- Smoking/tobacco use
- Passive smoking
- Radon/other radiation exposure
- Exposure to:
- Arsenic/asbestos
- Coal smoke/vehicle exhaust
- Silica/rock dust
- Nitrogen oxides
(b) Tumour vs normal tissue differences:
- Fewer/smaller alveoli or air spaces
- Higher cell density (more nuclei per area)
- Increased mitotic activity
(c) Rapid-growing tumour prediction:
- Observation: More cells in mitosis (prophase/metaphase/anaphase/telophase)
- Reason: Higher mitotic index due to uncontrolled cell division
▶️ Answer/Explanation
a.
- In 1950, the proportion of male smokers ≈ 80%
- In 2000, the proportion of male smokers ≈ 36%
- Change = 80% – 36% = 44%
b.
Similarity:
Both males and females show an overall decrease in smoking rates after around 1970
Difference:
- Males: Consistent decrease from 1950 onward
- Females: Increase from 1950 to ~1970, then a decrease
- Male smoking rate is always higher than female smoking rate
c.
- There is a positive correlation: Higher smoking rates are associated with higher mortality from lung cancer
- Male mortality peaks around 1960, even though smoking rates were already declining, suggesting a time delay between smoking and cancer development
- Cancer is known to take time to develop due to genetic mutations, hence lag effect
- Correlation ≠ causation: Other variables might contribute to cancer, though the pattern is strong
- The graph shows mortality from lung cancer, not incidence, which may slightly affect interpretation
d.
- Current smokers have the highest incidence of lung cancer (38.6%)
- Incidence decreases as the number of years since quitting increases
- Significant drop in lung cancer risk occurs within the first 10 years of quitting
- After 30+ years, risk is very low (6.3%), approaching that of non-smokers (0.7%)
e.
- The earlier a smoker quits, the lower their risk of lung cancer
- Current smokers have nearly 40% incidence, while those who quit ≥30 years ago have only 6.3%
- Risk drops significantly within 10 years of quitting
- After a long period of non-smoking, risk is almost as low as that of lifelong non-smokers
f.
- Asbestos
g.
- Emphysema
- Chronic bronchitis
Markscheme:
a. «-» \(44 \%\) \( \checkmark \)
Allow answers in the range of 43% to 45%
b. Similarity:
a. both show an overall decrease OR both decrease after 1970 \( \checkmark \)
Difference:
b. proportion of male smokers is always higher than female OR men decrease more OR women first increase «till 1970» and then decrease whereas men decrease throughout OR males highest value in 1950 and females in 1970 \( \checkmark \)
There should be one similarity and one difference
c.
a. more smoking leads to more deaths OR there is a correlation between smoking and deaths from lung cancer \( \checkmark \)
b. «nevertheless» male mortality peaks in 1960 when declining numbers of smoking \( \checkmark \)
c. cancer takes time to develop causing delay between changes in smoking and cancer \( \checkmark \)
d. correlation does not prove causation \( \checkmark \)
e. the data shows deaths from lung cancer, not incidence \( \checkmark \)
d.
a. highest incidence with continual smoking \( \checkmark \)
b. negative correlation/incidence decreases with length of time not smoking \( \checkmark \)
c. decrease «in incidence» occurs at less than 10 years since stopping smoking \( \checkmark \)
d. after 30 years incidence is not much more than non-smokers \( \sqrt{} \)
e.
a. incidence of lung cancer decreases the earlier the smoker gives up smoking \( \checkmark \)
b. continuing smoking increases incidence of lung cancer \( \sqrt{} \)
c. after 30 years of not smoking the risk of lung cancer is low/similar to non-smokers \( \checkmark \)
Accept vice versa
f. passive smoking/second hand smoke/exposure to radon/asbestos/pollution/smog/genetic predisposition \( \checkmark \)
g.
a. emphysema \( \checkmark \)
b. bronchitis \( \checkmark \)
c. COPD \( \checkmark \)
d. asthma \( \checkmark \)
e. pneumonia \( \checkmark \)
Only mark first two
▶️ Answer/Explanation
a.
Type I pneumocytes:
- These are extremely thin cells forming the majority of the alveolar wall.
- Their main role is to allow gases like oxygen and carbon dioxide to pass easily between the air in the alveoli and the blood in the capillaries.
- Their thin structure minimizes the diffusion distance, making gas exchange efficient.
Type II pneumocytes:
- These are larger, cuboidal cells found less frequently in the alveolar wall.
- They produce and secrete surfactant, a fluid that coats the inside of the alveoli.
- Surfactant reduces surface tension, preventing the alveoli from collapsing during exhalation.
- They also help repair damaged alveolar tissue and replace Type I cells when needed.
b.
- Oxygen movement: The concentration of oxygen is higher in the alveoli than in the blood arriving at the capillaries. Oxygen dissolves in the thin layer of moisture lining the alveolus, then diffuses across the alveolar wall and capillary wall into the blood. Once in the blood, it binds to hemoglobin in red blood cells, keeping the oxygen concentration low in plasma and maintaining a steep gradient for continued diffusion.
- Carbon dioxide movement: Carbon dioxide is more concentrated in the blood (coming from the body’s tissues) than in the alveolar air. It diffuses out of the blood, through the capillary wall and alveolar wall, and into the alveoli to be exhaled.
- The thin barrier formed by the alveolar and capillary walls, combined with a large surface area and constant blood flow, ensures gas exchange is rapid and efficient.
Markscheme:
a. Pneumocyte Functions:
Type I:
• Carry out gas exchange \(\sqrt{ }\)
OR
• Facilitate diffusion of gases (\(\mathrm{CO}_2\)/\(\mathrm{O}_2\))
Type II:
• Secrete pulmonary surfactant \(\checkmark\)
• Maintain alveolar fluid balance
b. Gas Exchange Mechanism [3]:
1. Oxygen exchange:
• Higher \(\mathrm{O}_2\) concentration in alveoli than capillary blood \(\checkmark\)
• Hemoglobin maintains concentration gradient by binding oxygen \(\checkmark\)
• \(\mathrm{O}_2\) dissolves in alveolar fluid \(\checkmark\)
• Diffuses through alveolar-capillary membrane into blood \(\checkmark\)
2. Carbon dioxide exchange:
• Higher \(\mathrm{CO}_2\) concentration in blood than alveolar air \(\checkmark\)
• \(\mathrm{CO}_2\) diffuses from blood into alveoli \(\checkmark\)
Note: Marking scheme requires 3 distinct points for full marks